Активация каналов акупунктуры при covid – 19 и ее другие возможности

Техника активации всей системы каналов акупунктуры разработана нашей группой еще в 2003-2004 году, а теоретическая работа, имеющая целью попытку объяснить, как это действует, опубликовали в Интернете еще в 2010 году, 

однако отсутствие ее востребованности за это время оставляло желать лучшего.

Из-за недостаточной изученности этих функций у человека мы не можем сказать, являются ли они более выраженными у населения России, что могло бы косвенно объяснить относительно низкую заболеваемость COVID – 19 на территории России, или эти свойства присущи всем национальностям на Земле.

Однако, мы убеждены в том, что повышение активности этой системы достоверно помогает в лечении различной патологии, в том числе патологии сердечно-сосудистой системы, патологии органов дыхания, улучшении течения сахарного диабета и других заболеваний, в том числе COVID – 19, а при эпилепсии в подавляющем большинстве случаев оказывает исцеляющее воздействие.

 

 На основании известных ныне фактов известно, что и шизофрения, и рак, и большинство других болезней содержатся в генотипе как спящий материал, который начинает работать в неблагоприятных условиях.

Точно так же на фоне депрессии, проявившейся в результате страха во время эпидемии, появляется дефицит эндорфинов и дофамина, а это осложняет течение заболевания из-за снижения неспецифической резистентности организма. Психологический шок отнюдь не способствует лучшему состоянию пациентов, но значительно  усугубляет прямые шоковые реакции, развивающиеся от действия патогена. Активное состояние системы каналов акупунктуры дает организму дополнительный запас прочности, и поэтому люди даже и не узнают, что перенесли такое грозное заболевание, как COVID – 19, отделавшись легким ОРВИ.

Благодаря изучению особенностей заболевания COVID – 19, мы хотим привлечь внимание ученых и врачей к положительному воздействию активации системы каналов акупунктуры человека. Кроме того, в свете этого проясняются и эффекты многих других лечебных воздействий и психологических методик лечения соматических заболеваний.

  Летальность от COVID – 19 в мире

Летальность очень сильно отличается в разных странах.  

· США – 5,36%

· Италия – 13,22%

· Великобритания – 13,2%

· Франция – 12,8%

· Испания – 10,29%

· Китай – 5,53%

· Германия – 3,2%

· Иран – 6,3%

· Швейцария – 5,0%

· Южная Корея – 2,2%

· Нидерланды – 6,32%

· Австрия – 3,05%

· Бельгия – 3,96%

· Канада – 4,5%

· Португалия – 3,5%

· Бразилия – 6,4%

· Россия — 0,85%Украина – 2.61%

Вероятно, разница в смертности в разных странах больше зависит от индивидуальных и популяционных генетических особенностей, чем предполагалось, а так же зависит от организации социальной среды.

                                                  

Литература:

     Этан Уоттерс, «Эпигенетика», журнал «Гео», №7, 2007;

А.С.Мыльникова, «Психосоматические факторы при аллергии»,

ЗАБГГПУ, г.Чита, 2008;

 Stux Stiller Potsmann Jayasuriya,”Lehrbuch der kliniscen

     Acupunktur”, изд. Springer-Verlag, Berlin Heidelberg New York, 1981;                           

 

          https://arbalet.okis.ru/file/arbalet/reflexoterapia.DOC

          https://arbalet.okis.ru/file/arbalet/referat.DOC

          https://www.medrxiv.org/content/10.1101/2020.02.06.20020974v1.full.pdf

          https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.14238

          https://ohranatruda.ru/news/898/587274/

                https://ru.wikipedia.org/wiki/%D0%A2%D0%BE%D0%BA%D1%81%D0%B8%D0%BA%D0%BE%D0%BB%D0%BE%D0%B3%D0%B8%D1%8F_%D1%8D%D1%82%D0%B0%D0%BD%D0%BE%D0%BB%D0%B0

https://journals.lww.com/cmj/Abstract/publishahead/Analysis_of_factors_associated_with_disease.99363.aspx

https://ru.wikipedia.org/wiki/%D0%A4%D0%B0%D0%B9%D0%BB:Renin-angiotensin-aldosterone_system_rus.png

https://www.krasotaimedicina.ru/diseases/zabolevanija_pulmonology/tracheal-dyskinesia

https://www.krasotaimedicina.ru/diseases/rheumatology/connective-tissue-dysplasia

http://xn----7sbabkdpwufdsp9apq.xn--p1ai/crom

https://www.rlsnet.ru/mnn_index_id_2007.htm

http://lifebio.wiki/%D0%B0%D0%BD%D0%B3%D0%B8%D0%BE%D1%82%D0%B5%D0%BD%D0%B7%D0%B8%D0%BD%D0%BF%D1%80%D0%B5%D0%B2%D1%80%D0%B0%D1%89%D0%B0%D1%8E%D1%89%D0%B8%D0%B9_%D1%84%D0%B5%D1%80%D0%BC%D0%B5%D0%BD%D1%82

https://helix.ru/kb/item/1384

https://fb.ru/article/435420/angiotenzinprevraschayuschiy-ferment-pokazaniya-norma-prichinyi-povyisheniya-i-ponijeniya

http://journal.ukrcardio.org/cardio_archive/2004/2/vinogradova.htm

https://pneumoniae.net/rzhavaya-mokrota/

https://koronavirustoday.ru/info/smertnost-ot-koronavirusa-kakoj-realnyj-proczent-v-raznyh-stranah/

https://ecuro.ru/article/zabolevaemost-rakom-predstatelnoi-zhelezy-v-rossiiskoi-federatsii

https://academic.oup.com/jtm/advance-article/doi/10.1093/jtm/taaa041/5809509

                                                       27 апреля  2020 года

                                                       Город Чита, Забайкальский край, Россия

                                                   СГ «Родная Земля»

                                                       Мыльникова Марина Сергеевна

Native Land Citizens' Union to help socially

disadvantaged residents of the region

Pathogenesi reviews

COVID – 19

Performed by Mylnikova Marina

Chita City, Sabaikal Region, Russia

April 27, 2020

Content

1) Введение……………………………………… ………………….стр.3.

2) Angiotensining enzyme and its genetic features affecting the course of COVID - 19................................p.3 ……………………………..стр.3

3) Why enzymeactivity can be increaseda..........p.5

4) Нарушения свертывающей системы крови………………… стр. 9

5) Кашель при COVID – 19……………………………………….стр.10

6) Disruption of kidney function in the treatment of IAPF.............p.13

7) Angioeurotic swelling when takingIAPF................p. 13

8) Hematologicaleffects.......................................... page 18

9) The link between coronavirus disease and racialtraits...... p.20

10) Связь тяжелого течения COVID – 19 с некоторыми группами крови……………………………………… …………………… стр.21

11) Никотин и COVID – 19………………………………… стр.24

12) Vulnerability of young, physically strong people...... p.30

13) 19Эндорфины в механизмах защиты при COVID-19……. стр.31

14)Защитное участие дофамина в патогенезе COVID – 19….стр.34

15)Алкоголь и COVID – 19……………………………………… стр.35

16)Синкопальные состояния при COVID – 19………………. ….. стр.36

17)Sex andcoronavirus............................................. page 38

18)Стресс и течение COVID-19…………………………………..стр.38

19)Activation of acupuncture channels at COVID - 19 and its otherfeatures................................................ p.39

20)Летальность от COVID – 19 в мире………………………….. стр.40

21)Литература……………………………………… ……………... стр. 41

Introduction

This work is intended both for practitioners who protect the lives of patients with coronavirus infection at the forefront of the fight, and for scientists looking for effective treatments and medicines against COVID - 19.

The red thread this time will be the positive effect of activation of the acupuncture channel system and the factors affecting this process. Describing the effects of activation of acupuncture channels andbalancing the balance of ACE2 with the helpof other defense mechanisms largely explains why batsget alongpeacefully with coronavirus in their bodies.

Angiotensin-turning enzyme and its genetic featuresthat affect the course of COVID - 19

Since there is no comprehensive extensive research on this issueyet, here are quotes from availablesources.

Angiotensin-turning enzyme (ACE). Identification of the Alu Ins/Del mutation (regulatory gene area)

Название гена – ACE OMIM +106180

Gene localization on chromosome - 17q23.3

Gene function The ACE gene encodes angiotensin-transforming enzyme (ACE), a protein circulating in the extracellular space (carboxypeptidase) that plays an important role in regulating blood pressure and electrolytebalance, catalyzing the fission of inactive angiotensin I to active angiotensin II.

Alu Ins / Del

ACEIn the 16th intron of the ASE gene, an insertation-dividing (I/D) polymorphismwas identified ininsertion (inspection, I) or loss (division, D) of Alu-repeat, the size of 289 pairs of nucleotides.. Possible genotypes

§ I/I

§ I/D

§ D/D

Association of marker with diseases

§ Myocardial infarction,

§ coronary heart disease,

§ ischemic stroke,

§ Alzheimer's disease,

§ chronic renal failure, § остеопороз,

§ age-related macular degeneration,

§ Atherosclerosis.

General information about the study

Renin-angiotensin system (ASD) is involved in the regulation of blood pressure in humans.

The work of ASD is closely related to electrolytes, they support homeostasis, which is necessary for the regulation of cardiac function, fluid balance and many other processes. One of the components of the RAS system is the hormone angiotensin II, which causes vascular narrowing, increased blood pressure and is the main regulator of aldosteronesynthesis, formed in the tuber area of the adrenal cortex, the only result of this action is an increase in the volume of circulating blood and an increase in systemic blood pressure.

Conversion of inactive angiotensin I (is a decapitation - a sequence of 10 amino acids Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-Leu-Leu) into an active octap Eptic angiotensin II (by removing 2 amino acids-His-Leu) controls angiotensin-transforming enzyme (ACE) - a protein circulating in the extracellular space (carboxypeptidase). The second important function of ACE is the deactivation of bradytinin.

In addition to regulating blood pressure, ACE is involved in various processes occurring in the body. It is synthesized by cells of many tissues, such as vascular endothelial cells, renal epithelial cells, Leidig testicular cells, etc.

Normally, different people's LEVEL of ACE in blood plasma can vary up to 5 times. For a particular person, the level of ACE is quite stable. Such fluctuations in the level of ACE between people are caused by the polymorphism of the ACE gene. In the 16th gene intron, an insertation-dividing (I/D) polymorphism was identified in insertion (inseries, I) or loss (division, D) of Alu-repeat, the size of 289 pairs of nucleotides.. The division of Alu-repeat leads to increased expression of the ACE gene and increased concentration of ACE in the blood, lymph and tissues, which is a factor that increases the risk of cardiovascular disease (myocardial infarction, left ventricular hypertrophy, coronary heart disease), kidney disease, atherosclerosis, Alzheimer's disease. In persons who are homophobia D аллелю (genotype D/D), the level of ACE is increased by 2 times compared to I/I genotype.

The association of polymorphism with age-related macular degeneration (AMD) - the main cause of vision loss in old age - has been identified. The I/I genotype is 4.5 times more common in healthy people than in patients with AMD, and appears to protect against AMD.

Associations of asce polymorphism with the level of systolic and diastolic blood pressure have not been identified, except in cases of a malignant form of hypertension (rapidly progressing and seriously occurring, with significant damage to kidney and retinal vessels), in which the D/D genotype is more common.

D-allele is also associated with the risk of developing nephropathy in diabetic patients.

Allele I is associated with increased resistance of the body to physical activity. Low bone mineral density and muscle weakness are the main risk factors for bone fractures in postmenopausal osteoporosis in women. It was found that the presence in the genotype of the woman allele I positively affects the effectiveness of muscle training (in patients with genotype I/I it was 2 times higher than in women with the genotype D/D) in response to physical activity, against the background of hormone therapy.

Studies also show that high-class athletes-stayers increased the frequency of allele I associated with endurance.

Why the activity level of the enzyme may be increased

For a long time, doctors could not accurately name the reasons why some people have excessively elevated levels of ACE, while others do not have any problems with this enzyme. However, recent studies of geneticists in this direction have revealed the gene angiotensin-turning enzyme. It is the so-called ACE gene, which appears due to a small mutation and causes an increased synthesis of ACE in the body. This gene contributes to the appearance of not only high blood pressure in humans, but also many other cardiovascular pathologies. This pathology can manifest itself at any age. However, the researchers are very cautious to draw any conclusions from their discovery, as repeated experiments have yielded very contradictory information. In particular, some scientists found that ACE levels were dependent on gender or race, while others did not. Therefore, scientists suggest that for more accurate results of research may require an additional criterion to weed out the factors that influence the course of the experiment. - Victoria Ulasevich October 29, 2018 - Read more on FB.ru: https://fb.ru/article/435420/angiotenzinprevraschayuschiy-ferment-pokazaniya-norma-prichinyi-povyisheniya-i-ponijeniya

The norm of angiotensin-turning enzyme To interpret the results of the analysis, you need to know normal values for the enzyme. The analysis should show the results displayed in units of the ed/l. Enzyme standards in patients of different age categories differ. The value for children under the age of 12 is between 9.4 and 37/L. Teenagers 13-16 years of age have a little less active ACE in the blood.

For them, the norm is from 9.0 to 33.4 units/l. For adults, good values are considered from 6.1 to 26.6 ed/l. - Read more on FB.ru: https://fb.ru/article/435420/angiotenzinprevraschayuschiy-ferment-pokazaniya-norma-prichinyi-povyisheniya-i-ponijeniya

In 1990, the polymorphism of the ACE gene associated with insection (I) or division (D) in the 16th intron of 287 pairs of nucleotides was discovered. This polymorphism was associated with the level of ACE in the blood plasma, the higher it was in homozigote on the alley D. Thus, in the study of 80 healthy individuals it is shown that the level of ACE in the blood of carriers of genotypes II, ID and DD is significantly different and is 2 times higher than in patients with genotype II/ ID. (http://journal.ukrcardio.org/cardio_archive/2004/2/vinogradova.htm)

The ACE gene is mapd in chromosome 17q23. Presence or absence is used as a marker of polymorphism of the ACE gene (division/insertion; D/I) 287bp fragment in 16 gene intron. This polymorphism is not structural, but apparently affects the degree of expression of this gene. This is confirmed by a number of studies which have shown that in healthy individuals with DD genotype the maximum blood ACE level is determined, in people with the II genotype the level of blood ACE is half lower, and heterozygote blood enzyme intermediate level (Rigat B.1990). (http://www.rusmedserv.com/cardio/gen.htm

In the ELSA study, 320 patients with arterial hypertension in patients with DD genotype found a reliably high thickness of the IM carotid arteries and a higher prevalence of atherosclerosis of carotid arteries, compared to patients with II and ID genotype. Also interesting is the work of Amant and co-authors, who analyzed the risk of restenosis after stenting in 146 patients of coronary heart disease, depending on the genotype. According to the semi-annual observation in patients with DD, the genotype had the greatest degree of decrease in coronary avetaration according to the quantitative coronary artery. (http://www.rusmedserv.com/cardio/gen.htm

The level of angiotensin-transforming enzyme in the blood, lymph and tissues correlates with the presence of D allele. Concentration of ACE in serum in healthypeople, homozigoths by D allele,, almost twice as high, than in the homozigoths on the I allele and has an average value in heterozygous - ID genotype. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695206/

According to the same literature, the association of ACE D allele with the increase in diastolic pressure was established in the Freemangam study of a fairly

large population, however, was present only in men. In women, such a pattern was not observed. Ace polymorphisms were paired with abdominal obesity (table 2) of Pearson's χ2 (p 0.030), plausibility (p 0.024). The bond was linear (p q 0.010), symmetrical, medium-strength (γ 0.53; p q 0.004). Here, as well as in hypertension, there was a tendency to reduce the allele of wild type I and increase allele D in the presence of abdominal obesity (AO) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695206/

. Genetic predisposition to AG manifests with the age of man: as the age of age increases the proportion of patients in whom AG has a secondary character - patients with metabolic syndrome, atherosclerosis, renal pathology, which as the disease progresses join pathogenetic mechanisms of the development of AG. that DD genotype in the development of AG is more important in young people. The author explains the phenomenon of the accumulation of the trait by the phenomenon of accumulation of DD in the 2nd group. and 21.6% of patients with hypertension at the age of 35-48. The author attributes the less-than-possible occurrence of this genotype in the 3rd age group to the possible greater lethality after myocardial infarction, as well as "dilution" by the accumulation of those patients whose polymorphism of the ACE gene in the development of AG is of less importance. http://journal.ukrcardio.org/cardio_archive/2004/2/vinogradova.htm

The fact that people with hypertension are more likely to suffer from severe and complicated forms of DD COVID - 19 is also due to the same cause.

Genetic predisposition to AG manifests with the age of man: as the age of age increases the proportion of patients in whom AG has a secondary character - it's patients with metabolic syndrome, atherosclerosis, renal pathology, which as the disease progresses join pathogenetic mechanisms of development of AG. Thus, the paper notes that the DD genotype in the development of AG is more important in young people. 44.4 and 19.1%. The author explains the higher occurrence of the DD genotype in the 2nd group by the phenomenon of the accumulation of the trait. This assumption is confirmed by the fact that the DD genotype was found in 36.5% of patients who had hypertension before the age of 35, and in 21.6% of patients who had hypertension at the age of 35-48 years. The author attributes the less-than-possible occurrence of this genotype in the 3rd age group to the possible greater lethality after myocardial infarction, as well as "dilution" by the accumulation of those patients whose polymorphism of the ACE gene in the development of AG is of less importance. (http://journal.ukrcardio.org/cardio_archive/2004/2/vinogradova.htm

These data reveal the link between the DDgenotype that accumulates with age with the distribution ofmortality in the age groups.

The mortality rate of coronavirus, i.e. the proportion of deaths from all infections, is 1.29% (if it is true that 40% of the population has been infected in seven municipalities). The simultaneous accounting of "undiagnosed" infected and deceased has established a division into age-related risk groups. A country where all "receptive" people, i.e. 70% of the population or more, risk losing up to 1% of citizens is large (4.25%).

Another study on the treatment of hypertension in diabetic patients noted the following. Genotypes I/D and D/D prevailed in the groups of patients for whom the inhibitors and ACE therapywas effective,while in the group of patients for whom the therapy of this group was ineffective, the predominance of the I/I genotypewasexpressed. that the genotype I/I of the ACE gene is characterized by relatively low activity of ACE in blood plasma, while the D/D genotype is characterized by high enzyme activity in tissues and blood. https://cyberleninka.ru/article/n/polimorfizm-gena-ase-i-ego-vzaimosvyaz-s-effektivnostyu-medikamentoznoy-terapii-ingibitorami-apf-u-bolnyh-saharnym-diabetom-tipa-2-i

So, we can judge by the degree of exposure to ACE inhibitors whether, predominantly, which genetic type presused in a group of people.

There are many studies of the frequency and severity of IPF side effects. в осложненных случаях при коронавирусной инфекции.

Disturbances in the blood clotting system

The decrease in the prothrombin index indicates an acceleration of clot formation in patients with DD genotype. (Perhaps, in the case of COVID 19, this group will have an earlier clotting disorder.) Confirmation is the increase in FMC, indicating an increase in plasma complexes of fibrin-monomers with products of degradation of fibrinogen. In this case, the increased level of angiotensin II, caused by the implementation of the mutant homosigotic genotype in the form of an increase in the concentration of ACE in the blood, should induce the production and secretion of adhesive molecules, stimulate the formation of free radicals, which leads to the activation of the function of thrombocytes, including the suppression of nitrogen activity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695206/

Кашель при COVID – 19

the use of ACE inhibitors by origin is associated with a deficiency in the consumption of ACE2. The causes of this cough are closely related to the genetic polymorphism of ACE2. Without symptoms, many people get sick because a large part of the population has the ACE2 DDgenotype.

Japanese scientists studied the effect of ACE inhibitors on cough development depending on I/D polymorphism of the ACE gene. The study included 20 healthy individuals with genotypes II and DD (10 participants in each group) who took an acet cilasipril inhibitor for 4 weeks. The incidence of coughing in these groups varied considerably. The skin reaction to intracutaneous administration of bradytinin, which in carriers of genotype II significantly increased after the use of the ACE inhibitor, and in individuals with the DD genotype practically did not change. Thus, carriers of genotype II are more predisposed to the development of cough when using an ACE inhibitor, and this is associated with a change in the tissue level of bradytinin. (http://journal. ukrcardio. org/cardio_archive/2004/2/vinogradova. htm)

Thus, the analysis of these literature shows that the majority of researchers who studied the relationship of I/D polymorphism of the ACE gene with ad level and the development of AG, consider allele D associated with this pathology.2, 10, 13, 21, 27, 32, 36, 38, 42. Someofthe authors associate with AG allele I, others believe that only a combination of polymorphisms of different genes has a diagnostic value. in a number of papers, there is no association I/D of the polymorphism of the ACE gene with AG. 25, 52, environmental factors (particularly, as shown in the work,50) in high altitude conditions associated with hypoxia, allele I can give benefits in physical endurance); gender also affects the association of I/D polymorphism of the ACE gene with AD. (http://journal.ukrcardio.org/cardio_archive/2004/2/vinogradova.htm)

Thus, the incidence of coughing in people of different races has revealed a more frequent coughing in black people. Belonging to certain races (negro and yellow) is a risk factor for coughing against the background of IPF therapy. (Also, black and yellow race is currently a risk factor in COVID - 19.) For example, a study conducted in Hong Kong in sick Chinese with heart failure, found that persistent cough develops in 44% of IAPF recipients (in 46% of patients receiving captopril, and in 41.8% of patients receiving enalapril).

The reason for the racial differences in the frequency of coughing in the background of IAPF therapy is not exactly established. Racial differences in pharmacokinetics and pharmaceutical dynamics of IPF, as well as the sensitivity of the cough reflex, are discussed.

In patients with CSN cough develops reliably more often than in patients with arterial hypertension, in 26% and 15% of cases, respectively. Cough, caused by IPF, in CSN usually appears earlier than in hypertension.

It is believed that none of the hypotheses about the causes of coughing on the background of therapy IAPF can adequately explain the nature of this side effect. (We assume that cough is a marker of the resulting ACE2 deficiency.)

The most common mechanism is considered to be the increase against the background of the inhibition of ace level of bradytin.

Inhibition of ACE in the lungs can lead to the accumulation of bradytinin in the upper respiratory tract, contributing to the development of cough. Bradyconine stimulates non-myelinated afferent sensitive C fibers by influencing the J-type receptors involved in cough reflex. (Below, we will look at the evidence that the breakdown of inertia has dyskinesia syndrome of the trachea and bronchi.)

Degradation of substance P - a neurotransmitter for afferent sensitive nerves, and especially C fibers - is also carried out at the expense of ACE. Therefore, the inhibition of ACE may be accompanied by an increase in the influence of this substance. The synthesis of prostaglandin E, caused by bradykinin and substance P, can have broncho-constirtoric action.

It is assumed that there is a genetic predisposition to the development of cough on the background of IPF therapy. A study of the polymorphism of the ACE gene found that about 16% of people are homophobia on the long alley of this gene. So the incidence of coughing among patients,Patients who are homozigotes on this allele have lower concentrations of ACE. (It also proves that coronavirus can cause a deficiency in THEF2 consumption, especially in those people who have a factor of reducing ACE2 - the reception of ACE Igibitors.)

Cough is usually dry, jerky, long-lasting and paroxysmal. It can strengthen in a horizontal position and be so strong that it causes ochriplation, vomiting and urinary incontinence at the time of coughing. Coughing is not accompanied by a significant change in lung function, signs of bronchial obstruction or hypersensitivity. The appearance of cough is probably independent of the dose of IPF, and it can occur at low doses. However, one study noted that lowering the dose of IAPF leads to a decrease in the severity of coughing. Coughing is so pronounced that it affects the patient's consent to continue tr

gainst the background of IPF, the quality of life is worse, and the level of depression is higher compared to patients who did not have a cough. (Indirectly, this may suggest that there is a shortage of endogenous opiates in this category.)

The pathogenetic treatment for cough will be sodium Cromoglicate. It inhibits both early and late stages of allergic reaction, preventing the degranulation of mast cells and the release of inflammation mediators (histamine, bradykinin, slow-reactioning substance, leukotrien, prostaglandins). Due to these properties, Intal prevents bronchospasm caused by contact with an allergen or other provoking factor (cold air, physical tension, stress). In addition, it reduces the intake of other anti-asthmatic drugs (broncholytics, glucocorticosteroids). (https://medi.ru/info/11659/

Disruption of kidney function in the treatment of IAPF

All IPF, inhibiting the synthesis of angiotensin II in the kidneys, can cause deterioration of kidney function. However, in most cases it is asymptomatic and reversible. Kidney dysfunction caused by IPF in many cases does not progress, despite the continuation of IPF therapy.

Long-term congestive heart failure itself is often accompanied by a significant deterioration in kidney function, so it is not always easy to distinguish the negative impact of IPF on kidney function from renal dysfunction caused by the underlying disease. Still, in some cases, the effects of kidney damage caused by IAPP therapy can be severe and even life-threatening.

The deterioration of kidney function (increased levels of creatinine plasma by more than 0.5 mg/dL) occurred in 16% of patients in the enalapril group and 12% of patients in the placebo group, i.e., patients receiving enalapril had a 4% greater chance of developing kidney dysfunction. In multivaration analysis of older age, diuretics therapy and diabetes were factors contributing to lower kidney function against the background of IAF treatment, while therapy with z-blockers and higher FI LM acted as renoprotective factors. https://medi.ru/info/11659/

Angioeurotic swelling at IPF

This side effect occurs at a frequency of 0.1-0.3% and is a potentially life-threatening side effect.

This complication is usually manifested by local swelling of the lips, tongue, mucous oral cavity, larynx, nose and other parts of the face.

The mechanism of development of this side effect of IPF is associated with the action of bradytinin or one of its metabolites. Angioeurotic swelling may be caused by the production of prostaglandins, which cause the release of histamine.

Thus, this side effect is a manifestation of the pharmacological action of IAPF, which may become redundant in individuals with genetically hypersensitivity.

All IAPF can cause this complication. More often it develops at the beginning of IAPF therapy, but can also appear with long-term treatment. In the analysis of 163 reports of the development of angioeurotic edema against the background of IAPF therapy in 21% of patients, it developed within 24 hours from the beginning of treatment, and in 20% - after 6 months. And more. On average, the development of angioeurotic edema was observed in 3 weeks. from the beginning of therapy.

Angioeurotic swelling was also noted against the background of the treatment of IAFF with the safest profile - perindoprol. Although the frequency of its detection in the analysis of data of 47,351 patients with arterial hypertension, participated in the post-marketing study, was low and was only 0.006%, in the treatment of 320 patients with CSN it reached 0.3%. There is evidence of a greater predisposition of black people to the development of angioeurotic edema, which is consistent with data on racial differences and in the incidence of other side effects of IAPF. (And this is also consistent with data on a higher incidence of complications in COVID - 19 in black people..)

Usually this complication is manifested by moderate symptoms, which takes place within a few days after the termination of IAPF therapy.

However, in rare cases, angioeurotic swelling may manifest symptoms such as respiratory distress syndromecaused bylaryngospasm, And, even with the development of pronounced angioeurotic edema caused by IAPF therapy requiring treatment in the intensive care unit,in most cases the relationship of swelling with IAPF therapy is not recognized, especially when angioeurhetic swelling develops at the distant onset of IAPF therapy. Butthe authors point out that so, in the analysis of 4,970 cases of angeureurous swelling, which is caused by IAPP therapy, is higher than is generally believed.

The rare localization of angioeurotic edema includes small intestines. Angioeurotic swelling of the intestine can develop both in combination with swelling of the face and mouth, and in the form of isolated visceral angioeurotic edema.

Chase M.P. et al. (38) describes two episodes of this complication in a 72-year-old woman who complained of abdominal pain, vomiting and diarrhea.

A CT scan during both episodes revealed swelling of the small intestine wall. Analysis of anamenetic data showed that for 1 monthon the firstepisode, the patient began treatment with lysinopryl, the dose of which increased 24 hours before each episode of angioneurotic edema.

Patients who have experienced angioeurotic edema of any severity (including mild symptoms) should not receive IPF therapy in the future.

Patients indicating idiopathic angioeuurotic swelling in history may have an increased risk of developing this complication when taking IPF. https://medi.ru/info/11659/

The manifestations ofangioeurotic edema correspond to the clinic of COVID. Что есть общее? most complications tooronavirus infection.

1) Cough occurs in coronavirus and taking ACE inhibitors. This cough is much more common (44 -46%) occurs in people of yellow and black races, and these same races are more likely to experience complications and death.

2) Skin rash occurs there and there, and similar in appearance. The high incidence of skin rash has been identified in initial studies of captopril. However, it was thought that the high incidence of the rash in these studies was most likely due to a large dose of captopril (600-1200 mg/sou). (The fact of detecting a rash when receiving too much dose indirectly indicates a deficiency of ACE2 in the case of COVID – 19.)

The rash occurs in 1-5% of patients receiving IPF for arterial hypertension. The skin rash caused by IPF therapy is in most cases an itchy maculopulopulsal rash that is located on the arms and upper body. The rash usually develops during the first 4 weeks. (most often during the first few days). The rash is more often transient, persisting only a few hours or days, so its appearance does not always require the cancellation of the IPF.

3) Respiratory distress syndrome can be both in coronavirus and when taking IPF. Angioeurotic swelling was also noted against the background of the treatment of IAPF with the safest profile - perindoprol. participated in the postmarketing study was low and was only 0.006%, in the treatment of 320 patients with CSN it reached 0.3%. (This is also consistent with data on relatively high mortality among black people in COVID - 19.)

Usually this complication is manifested by moderate symptoms, which takes place within a few days after the termination of therapy IPF, although in rare cases can lead to death.

4) Abdominal pain, vomiting and diarrhea - can also be in both cases. Rare localization of angioeurotic swelling includes small intestine.

Chase M.P. et al. (38) describes two episodes of this complication in a 72-year-old woman who complained of abdominal pain, vomiting and diarrhea.

A CT scan during both episodes revealed swelling of the small intestine wall. Analysis of anaamnestic data showed that for 1 month. Before the first episode, the patient began treatment with lysinopril, the dose of which increased 24 hours before each episode of angioeurotic edema. After the cancellation of the IAPF, episodes of angioeurotic swelling were not repeated during 1 year of observation.

5) The drop in pressure and shock reactions may be the same as due to the use of IAPF, and in the case of COVID - 19. All IAPF can cause arterial hypotension.

Although the development of hypotension in the treatment of IPF is usually associated with the first dose, it can appear at later stages of therapy. Reduced blood pressure after taking the first dose is usually small and asymptomatic, which does not lead to a violation of perfusion of vital organs. However, a small number of patients may have severe hypotension, accompanied by symptoms of hypoperfusion of the heart, brain and kidneys.

6) Disturbances of taste and smell are typical for both coronavirus and IPF. ACE inhibitors sometimes cause impaired taste sensitivity (dysgeusia). This effect is variously described by patients as loss of taste, appearance of a metallic taste, appearance of sweet taste or perversion of taste. The incidence of taste sensitivity disorders when taking captopril in doses less than 150 mg/day is from 0.1% to 3%, and at doses of more than 150 mg/day increases to 7.3%. contained in the captopril molecule, these disorders occur against the background of enalpril and lysinopril therapy, which do not contain this group.

This suggests that this side effect may be common to all IAPF.

7) Неврологические нарушения.

8) Peppering and scratching in the back wall of the throat is also typical for the reception of IAPF, and for coronavirus.

9) Particularly similarity is evident in the fact that angioeurotic swelling, one of the consequences ofwhich is respiratorydistress syndrome, is most common in people of

black and yellowraces, and we know that these races are prone to complications and death in coronary disease.

And all these symptoms occur when taking ACE inhibitors in therapeutic, that is, small doses. And when you consider that the coronavirus rapidly reproduces and consumes this very important enzyme, it becomes clear why people fall into such terrible states, dangerous to life.

Hematological effects

ACE inhibitors usually cause a slight decrease in the level of hemoglobin and hematocrit, which for most patients is not clinical. Cases of aplastic anemia against the background of captopril therapy are described. It was also reported that the development of aplastic anemia in two patients in the treatment of lysinopril at a dose of 5 mg per day; in both cases, the patients were elderly and elderly (64 and 79 years old). The development of aplastic anemia in one case is observed after 6 months. from the beginning of treatment with lysinopril, and in another - after 15 days. After kidney transplantation, anemia caused by taking IPF is most likely to develop due to a decrease in erythropoietin levels.

Neutropenia and agranulocytosis are relatively rare side effects of IAPF therapy. With the use of high doses of captopril (150 mg per day or more) and in severe patients, the frequency of neutropenia increases. Thus, in patients with normal levels of creatinine plasma and lack of diffuse diseases of connective tissue, the incidence of neutropenia on the background of captopril therapy was 0.02%, and in patients with systemic lupus erythematosus or scleroderma with an increase in creatinine levels of zgt;177 mcmol/l it increased to 7.2%. Other autoimmune diseases also increase the risk of neutropenia caused by IPF. This is probably due to the ability of IPF to induce the formation of antinuclear antibodies. Neutropenia, which has a probable autoimmune genesis, develops in about 7% of patients with autoimmune diseases receiving captopril. In addition, the risk of neutropenia increases with the simultaneous prescribing of cytostatics and captopril. It is also noted that a significant increase in the risk of granulocytopenation occurs with the simultaneous appointment of interferon and IAPF. (We see that autoimmune lesions are typical of both coronavirus infection and ACE2 deficiency caused by IPF. Therefore, it is probably quite wrong to take all the autoimmune effects developing with COVID - 19, only by the direct action of viruses, it is also the result of a deficiency of ACE2.)

It is interesting to read below the data on the appointment of interferon in coronavirus infection that Interferon can contribute to infection with coronavirus infection.

o

o MASSACHUSETTS, UNITED, STATES,, April 26, 2020,00:09 - REGNUM American scientists have investigated the mechanism of cell infection with a new coronavirus infection and found that interferon, which the body uses to stimulate immunity, can contribute to infection with the SARS-CoV-2 virus.

It is noted that a new coronavirus has previously been proven to penetrate cells using the ACE2 receptor and the TMPRSS2 enzyme. For example, ACE2 is used in the body to maintain the tone of blood vessels.

Researchers at the Massachusetts Institute of Technology found that only a very small percentage of respiratory cells (less than 10%) were in the respiratory system. ace2 receptors. But the most unusual thing was that the ACE2 gene, which encodes the receptor used by SARS-CoV-2 to penetrate human cells, is stimulated by interferon, one of the body's main defenses when the virus is detected. Interferon actually incorporates the ACE2 receptor at higher levels, providing the virus with new "portals" for penetration.

Thus, the use of interferon at the stage when the virus actively penetrates into human cells, can further aggravate its condition, conclude scientists.

Researchers suggest that the mechanism found also explains the emergence of a "cytokin storm" - an excessive inflammatory response that often kills people withCOVID-https://regnum.ru/news/innovatio/2929115.html.

Link of coronavirus disease with racial characteristics

The percentage of African-Americans among those infected with coronavirus and who died from Covid-19 is disproportionately higher than their share of the U.S. population as a whole, according to data in several U.S. states.

There are no complete statistics on the racial composition of Covid-19 Americans who have fallen ill and died; the federal Centers for Disease Control and Prevention (CDC) has not published such data (there are activists claiming that the federal government collects this information), has not yet disclosed its data and authorities to a number of states with large African-American communities and a large number of cases, including New York, California, New Jersey and Washington.

However, for example, from the statistics of illinois and the local metropolis of Chicago it is clear that from the new coronavirus blacks suffer noticeably more. Blacks make up 30 percent of Chicago residents. However, among those infected with coronavirus, half of them, and the proportion of the dead (as of Wednesday morning 118 people) is about 70%. In Illinois as a whole, blacks make up 15 percent of the population, but they account for 28% of confirmed cases and 43% of deaths.

A similar pattern is observed in Wisconsin, Michigan, Louisiana, North and South Carolina, writes the New York Times.

As Chicago Health Commissioner Allison Arvadi noted in an interview with the Washington Post, the life expectancy of black residents in the city is on average nearly nine years less than that of white Chicagoans.

Numerous studies show that the incidence of diabetes among black Chicagoans is twice as high as that of whites, and lung mortality is nearly 20% higher.

One in five African-Americans have high blood pressure, a quarter higher than white Chicago residents. Above, we quoted the results of studies that confirm the importance of racial differences in the formation of coughing when taking IPF, racial differences in the formation of AG, coronary heart disease, diabetes in connection with the characteristics of the PH2 genotype.

All these are risk factors that are statistically correlated with the severe course of Covid-19 disease. https://rus.postimees.ee/6945582/chernokozhie-v-ssha-umirayut-ot-covid-19-gorazdo-chashche-chem-belye-pochemu

Butit'snot just poor living conditions that are notjust about poor living conditions. More important is predisposition due to the genetic characteristics of ACE2, which

predominate among black people. This is clearly evidenced by studies of the frequency of side effects of IPF in thisgroup.

The connection of the severe current of COVID - 19 with some blood groups

Addictionis not only for COVID - 19, it is also in other diseases. In a number of cases, a link between blood group and risk of certain diseases (predisposition) has been identified.

According to research published in 2012 by a group of American scientists led by Prof. LouKiof Harvard Schoolof PublicHealth,individuals with blood type A (II), B (III) and AB (IV) have a greater predisposition to heart disease than those with group O (I): 23% for individuals with AB blood group (IV), 11% for individuals with blood group B (III) and 5% for individuals with blood group B (III)

According to other studies, people with b group B (III) have several times lower incidence of plague. There is evidence of a relationship between blood groups and the incidence of other infectious diseases (tuberculosis, influenza, etc.).

In persons who are homophobia on antigens (first) blood group 0 (I), 3 times more common stomach ulcers.

Blood-to-blood group B (III) has a higher risk of severe nervous system disease, Parkinson's disease.

British scientists from the Oxford Regional Blood Transfusion Centre were the first to become interested in clotting of different blood groups. In 1964, they examined blood samples from 232 men and 178 women, having previously divided them into two categories: Group I and all others (non-I).

The British hypothesis did not go unnoticed, and in 1975 Italian researchers decided to correlate different cardiovascular diseases with blood groups of patients. They analyzed data from 746 patients with hypertension (AG), 3,258 patients with congenital heart defects and 1,047 patients with acquired heart disease. Blood groups were classified under the AVO system. The results were mixed:

· arterial hypertension is more common in men with the second blood group, less frequently with III (which is interesting, this pattern was only seen in men!);

Myocardial infarction is much more common in patients with the second blood group, and less often with I (regardless of sexIn the mid-1980s, there was no

doubt that the second blood group has something to do with coronary artery disease. The answer was received by German scientists from the Institute of Gerontology in Nuremberg. The scientists fortunately excluded patients with each of these factors from the study and tested the distribution of blood groups among the remaining blood groups. After the last risk factor was excluded, the predominance of patients with the second group became even more pronounced than originally.

In 1990, scientists at the Royal Infirmary of Edinburgh went back to the theory and demonstrated how blood type can be a risk factor for cardiovascular disease. It has been suggested that between the "extended" olygosaccharide antigens and plasma cholesterol, the fact is that the superficial red blood cell antigens that determine the blood group are oligosaccharides, and the red blood band red blood cells have an additional carbohydrate subedicacion. These antigens are found in all tissues of the body, including in the endothelial vessels. The scientists found that, in addition to the increased concentration of the VIII clotting factor, the blood of non-I group patients had elevated cholesterol levels. They have a mutual influence, which explains the greater incidence of vascular pathologies in patients with non-I group.

In 1994, British scientists from St. Bartholomew's Hospital (London) published a 16-year-old observation of 1,393 men aged 40-64. During this time, 178 cases of coronary heart disease were recorded. Evaluation of the long-term results showedthat the IV blood group represented the greatest risk of developing coronary heart disease compared to other groups, especially in relation to death. In the same year, Polish scientists conducted another "purely masculine" study involving 200 men who underwent aortic coronary bypass surgery. The result is that the most common atherosclerosis is observed in patients with IV blood type. 2001: Pakistani researchers again provethat patients (by sex were not shared) with coronary heart disease and myocardial infarction II blood type is more common than others (and I - less often than others).

The "purely feminine" study was conducted by Lithuanian researchers in 2002. They observed 441 women suffering from atherosclerosis. Scientists have found that women with the third blood group are most likely to suffer, and I, on the

contrary, is associated with the lowest risk of atherosclerosis. No evidence of a link between II and IV blood groups with atherosclerosis in women was found... https://mylektsii.ru/8-9985.html

Doctors have been fighting over this problem for a long time, almost since the opening of blood groups. Numerousstudies from Europe, America and Asia, conducted since the second half of the last century, have been able to establish such a link.

The link between blood group and risk of developing GSD has been proven.

The connection is quite fully reflected in the literary review of Russian colleagues, built in chronological order, where later studies confirm the early ones..

I (0) группа:

Almost all researchers consider it the safest blood group for THE CCC.

II (A) group:

Its owners are more likely to suffer from hypertension, angina and myocardial infarction (research: Italy, 1975; Norway, 1980; Germany 1980; Pakistan, 2001; Taiwan, 2012; USA 2012). (And it has been found that people with a second blood type are more likely to get problems with COVID -19..)

III (G) group:

It contains a predisposition to the development of angina (USSR, 1978; England, 1990; Palestine, 2009).

IV (AB) group:

Increased risk of arterial hypertension (according to I.I. Sapozhnikov - by 46%; USSR, 1977), coronary heart disease (England, 1994; USA, 2012).

Patients in the non-0 group had elevated levels of blood clotting factors (the Willebrand factor and the VIII factor).

The excess level, according to various researchers, is 8-25 % of the level of group 0. This leads to hypercoagulation (increased clotting), thrombosis, and therefore to heart attack and stroke.

In addition, people with a II (A) group have higher levels of "bad" cholesterol fraction. And in the IV (AB) group increased propensity to develop an inflammatory process in the wall of vessels.

Based on this, it can be assumed that the increased risk of COVID - 19 in persons with the second blood group may be associated with the features of the clotting system of the blood, as a result of which there is a more frequent and pronounced formation of pneumonia and DVS syndrome.

Smokers develop physical addiction to the ingestion of nicotine in the body, which, firstly, reduced the synthesis of their own acetylcholine, and secondly, reduced the amount of H-cholineceptors, as excess intake of nicotine is subjected to compensatory regulation.

Tobacco smoking plays an important role in the formation of a pathogenic symptom. In most cases, small blood vessels, capillaries and small amounts of blood rupture occur. Since its volume is not large, in the absence of a large amount of mucus in the bronchi, the hematological fluid manages to fully oxidize, turning into iron oxide (own, rust).

Another reason may be to increase the permeability of capillaries in smokers. This is ubiquitous and the more often the more smoking experience a patient has.

The starting point of this topic was the information report of the European Journal of Allergy and Clinical Immunology, which mentioned the surveys of Chinese patients who contracted coronavirus at the dawn of the epidemic and the findings of a negligible percentage of smokers among the sick.

It is known that people who have problems with the respiratory system (asthma, allergies, COPD) are most prone to a number of viral diseases, which just "beat" on their weak place. Therefore, in the case of coronavirus, the results surprised the researchers. None of the COVID-19 patients suffered from asthma and allergies, and COPD (chronic obstructive pulmonary disease) accounted for only 1.4%.

Later inFrance, empirical evidence from Chinese scientists that smoking reduces the risk of infection and development of severe forms https://www.kp.ru/daily/27121/4204052/

The study involved 480 patients with a positive coronavirus test. The average age of patients treated in the hospital was 65 years. Of these, only 4.4% were heavy smokers. Among those who were treated at home, only 5.3% were smokers, and their average age was 44 years.

For comparison, in France between the ages of 44 and 53 smokes about 40%, and in the age group 65-75 years - about 11%.

After analyzing this ratio, the scientists put forward two theories. The first is that nicotine can prevent the body from being infected with coronavirus. Second, nicotine can protect the immune system from an overreaction to the virus. In both cases, nicotine can have a beneficial effect on the body when infected with COVID-2019.

The mechanism of the occurrence of such dependence was studied in detail by scientists from the United States, who found that in the human brain there are at least 5 types of nicotine acetylcholine receptors and each of them nicotine is affected by different degrees of severity. The highest sensitivity to nicotine is found in dopamine receptors, which provide a "sense of pleasure" in the human brain and they are "guilty" in the development of nicotine dependence. H-cholinoneceptors activate other reactions, as a result of which nicotine stimulates the release of dopamine, glutamine (the main excitatory substance in the brain), serotonin (the hormone "joy"), catecholamines (adrenaline and norepinephrine - hormones "stress"). This leads to a temporary increase in mood, improved cognitive function in the smoker, causes an imaginary surge of energy and energy. https://ne-kurim.ru/glossary/nikotinovye-atsetilkholinovye-retseptory/ https://yandex.ru/health/turbo/articles?id=6838&text=%D0%BD%D0%B8%D0%BA%D0%BE%D1%82%D0%B8%D0%BD+%D0%B8+%D1%8D%D0%BD%D0%B4%D0%BE%D1%80%D1%84%D0%B8%D0%BD%D1%8B&ids=6838&utm_source=yandex&utm_medium=search&utm_campaign=yandex-searchster&utm_content=article&saas_webreqid=1587896040221658-1539426537548387570500243-production-app-host-vla-web-yp-170

As for smoking, its deterrent effect is also likely to be associated not only with the content of single-valent metals in cigarettes such as potassium and sodium, but also with the fact that nicotine causes direct pharmacological erection of the penis and clitoris, and we are quite convinced of the positive effect of sex-related actions as helping to secretate endogenous opiates

and dopamine.

Pharmacological action - n-cholineimetic..

It interacts with peripheral (including those located in the synocototide zone, vegetative ganglia, adrenal brain matter and neuromuscular plates) and central n-cholinoceptors. In low concentration excites them, in high - blocks. In ganglia, the first phase (excitement) is associated with the depolarization of the membranes of ganglion neurons, the second (oppression) - with competitive antagonism with acetylcholine. In the central nervous system affects the content and modulates the release of acetylcholine, norepinephrine, serotonin and other mediators in the end of neurons. Reduces the secretion of STG and gonadotropins, increases - catecholamines and ADH. It promotes the release of endorphins. The effect on the cnness (arousal or oppression) depends on the doses, intervals between them

and the psychological state of the person. Small doses excite the central nervous system, including the vomit center. Nicotine can cause tremors and seizures. Stimulates the respiratory center (reflexively from the chemoreceptors of the synocarotide zone and directly).

Action on the cardiovascular system is caused by the activation of sympathetic influences: tachycardia (possible ventricular extrasystole), increased blood pressure, disruption of blood supply to organs and tissues (constriction of blood vessels), hyperoneuredinememia, increase of glycogenolosis, etc. Nicotine increases the release of the heart, increases the heart's performance and increases the consumption of oxygen myocardium. The activation of parasympathetic ganglia leads to an increase in secretion (bronchial glands and acidic gastric juice) and the tone of smooth muscles of the bronchus and gastrointestinal tract. It facilitates neuromuscular transmission. Increases the blood content of fatty acids and the adhesive ability of platelets.

The effect on the internal organs of small doses of nicotine entering the body during smoking is mainly due to reflex action (stimulation of the chemoreceptors of the carotid sinus and the arc of the aorta). Nicotine is gradually developing addiction.

In addition, smokers almost always have a spasm of bronchiol, because it is one of the effects of nicotine. Perhaps that is why coronavirus penetrates the alveoli of the lungs with difficulty in smokers and asthma patients, allergic rhinitis and atopic dermatitis, as well as with COPD, because these patients have signs of bronchial obstruction, which in this case turns out to be a physical obstacle to the penetration of coronavirus in the lower respiratory tract. However, with the development of pneumonia and complications, the condition will immediately deteriorate sharply, as lung tissue in smokers is affected by typical processes.

Another potential mechanism for the impact of smoking is the soot entering the airways. Hyaluronic acid, which sweats profusely in the alveoli when the lungs are edema, is foamed with breath, and this foam clogs the airways. Soot has the property to disturb surface tension, the smallest particles of soot, getting into the composition of sputum and mucus in the bronchi, disrupt foaming. It is also believed that smokers, due to the fact that the alveolar apparatus usually suffers, the alveoli are bloated, often occurs fibrosis, bronchoectase, it is difficult to talk about the complete preservation of receptors to ACE2

Pain relief

Systemic administration of nicotine causes the release of endogenous opioids (endorphins, enkephalins and dinorphins). In addition, the systemic administration of nicotine induces the release of methionine-encephaline in the dorsal horns of the spinal cord. Thus, nicotine has an acute neurophysiological effect, including an analgesic(antinociceptive)effect, and also has the possibility ofactivating the hypothalamic-pituitary-adrenal axis (GGN axis). α7 While the activation of the HGN axis is mediated by q4,2, but not by the researchers, this leads researchers to believe that the effects of nicotine on endogenous opioid systems are mediated by the 7, not the 4'2. Antagonist of opioid receptors - naloxone (NLX) - causes the withdrawal of nicotine after its re-introduction. NLX-induced nicotine withdrawal is inhibited by the introduction of the antagonist of the 7, but not the antagonist of the 4-2. The generalized evidence suggests that NLX-induced anesthesia and the development of physical dependence mediate endogenous opioid systems through q7 nAchRs..

Oxidative stress and apoptosis