Method of immune corrector therapy of myocardial infraction in rats

FIELD: medicine.

SUBSTANCE: modelling a myocardial infraction is followed by intravenous introduction of the immune corrector tamerite 3 mg/kg in an animal every days for seven days. The histological results of the myocardial tissue presented after the first, third and seventh days show the sufficiency and efficacy of the therapy.

EFFECT: effective therapy of the acute myocardial infraction ensured by reducing the intensity of an acute inflammatory reaction, providing faster granulation tissue formation.

2 tbl

 

The invention relates to experimental medicine, namely to the experimental form of myocardial infarction in rats, and can be used after myocardial infarction in rats for subsequent medical intervention and monitoring its effectiveness.

Myocardial infarction is one of the most frequent forms of diseases and is 3.9% among males and 2.2% among women, which puts it on one of the first places in the world. In Russia from myocardial infarction die 330 men and 154 women per 100 thousand population, which is 3.2 times more than in the US. These circumstances indicate a high relevance of the problem to THEM, in particular his treatment.

The Recommendations of the working group of the European society of Cardiology (2000) and based on them the Russian Recommendations (2001) the treatment of the developed myocardial infarction is based on the use of beta-blockers, nitrates, calcium antagonists and antiplatelet agents (aspirin, thienopyridine, antagonists of glycoprotein IIb/IIIA receptor of platelets). Despite the large number of different surgical and conservative methods of treatment mortality in acute myocardial infarction continues to be high: early complications lead to 10-15% of hospital mortality.

The main causes of death are developed is their heart failure and arrhythmias and conduction, due primarily to the value of developing myocardial infarction and progressive involvement in the process of intact cells of the myocardium. High mortality dictates the need to develop new treatments for this debilitating disease that would prevent the development or reduced the severity of these complications of myocardial infarction.

Modeling of acute myocardial infarction in rats, according to the authors, is the most reasonable, because these laboratory animals are similar to humans during physiological and pathological processes, which allows to use the results of animal studies to develop new methods of treatment of this disease in humans.

Known for the treatment of myocardial infarction drug atenolol, which has a complex mechanism of action: blocks beta-1-adrenergic receptors, which decreases the stimulating effect on the heart sympathetic innervation and circulating in the blood catecholamines, has antianginal, hypotensive and antiarrhythmic effect.

Introduction: a basic introduction is given intravenously in a dose of 5 mg, after 5 minutes, another 5 mg, then after an hour it starts taking the drug inside of 50-100 mg per day.

Disadvantage: the drug is contraindicated in bronchial obstructive syndrome, syndrome, sick sinus, Allocate and congestive heart failure; reliable performance in ischemia of repeated heart attacks and reducing mortality appears only in long-term care (about 2 years).

Sources of information

1. Selected topics in internal medicine. Ekaterinburg, 2007. Volume 4, p.101-172.

2. Drugs in Russia: a Handbook. M: Attraversare, 2003, p.3-1104.

Known drug acetylsalicylic acid, which is included in international and national recommendations for the treatment of myocardial infarction prototype.

Acetylsalicylic acid inhibits the activity of COX - the main enzyme of arachidonic acid metabolism, which is a precursor of prostaglandins, which provides anti-inflammatory, analgesic and antipyretic effects, and inhibits formation of THE, thereby inhibiting platelet aggregation.

Its positive side: with long-term use (at least 2 years) reduces the frequency of repeated heart attacks.

Negative sides: the drug is contraindicated in peptic ulcers, local bleeding, hemorrhagic diathesis; 40% of patients do not manifest antiaggregatory effect, considered to be the basic element protivoinfektsionnogo of action of the drug.

Sources of information

3. Selected topics in internal medicine. Ekaterinburg, 2007. Volume 4, p.101-172.

4. Drugs is Russia: a Handbook. M: Attraversare, 2003, p.3-1104.

An object of the invention is to increase the effectiveness of treatment of myocardial infarction using different chemical structure of the drugs with immunokorrektiruyuschie properties.

To solve this problem is proposed a method of treatment with immunomodulators myocardial infarction in rats after simulation-based medical intervention, characterized in that after creating a model of myocardial infarction is intravenous immunocorrector Tamarit in the dosage of 3 mg/kg every day for seven days with histological studies of myocardial tissue after the first, third and seventh days, and the results of these studies are judged on the adequacy and effectiveness of the treatment.

Known group of drugs belonging to the class of immunomodulators derived from different chemical groups, such as tumeric. The action of these substances differs from that currently used in medical practice drugs. So far not studied the effect in ischemic and acute phase of myocardial infarction. In this application described clinical trials of these drugs for the treatment of experimental myocardial infarction in rats. The effects of other imputation now being studied.

The treatment is the SL is blowing.

Modeling of myocardial infarction in rats, equal in severity with subsequent intravenous one group of animals compounds tamerica, with a study of indicators of cytolytic syndrome - transaminase and histological examination of the myocardium tissue is carried out within 7 days.

Influencing the nature of the acute inflammatory reaction (reducing intake of neutrophilic leukocytes that produce factors that stimulate inflammation, tumeric in the dosage of 3 mg/kg corrects for the acute phase of the syndrome of systemic inflammatory response, which leads to a decrease in the expression of leukocyte reactions, stimulates migration immunocompetent cells - lymphocytes, plasma cells, mast cells, macrophages in the necrotic foci, accelerates the formation of granulation tissue with proliferation of fibroblastic cells number and calls the substitution necrosis scar tissue, represented by the active fibroblasts and fibrous structures, without the effects of purulent inflammation of scar tissue.

Tracked action during acute phase of experimental myocardial infarction of tamerica in 50 cases.

The experimental results.

With Auntie the effectiveness and impact of immunocorrector of tamerica on blood biochemical parameters (M±m) in the dynamics of experimental myocardial infarction
IndicatorsIntact ratsDogs with experimental myocardial infarction
1st day IM5th day IM7th day IM
tumerictumerictumeric
(n=5)(n=5)(n=5)(n=5)
CPK (µmol/l-min)146,92±22,6323±43,79*405±of 27.84*291,35±18,90*
ACT (µmol/l-day)rate of 0.193±0,0140,254±0,0340,204±0,0290,177±0,024x
LDH1-2(µmol/l-day)165,15±34,6248,84±41,10*187,94±34,37
Note. The significance of differences of biochemical parameters in experimental and intact animals: * p<0,05, in animals treated with the drug t is merit x- p<0,05

Comparison histomorphologically data at different times of experimental myocardial infarction in the treatment immunocorrector timeritem
Time studiesTHEY have intact animalsTHEM animals treated with tumeric
1 days1. The damage zone is transmural nature, represented by cardiomyocytes events karyolysis, plasmolysis and plasmolysis.1. The damage zone is subepicardial character represented by cardiomyocytes events karyolysis, plasmolysis and plasmolysis.
2. Infiltration of the damaged area segmented by leukocytes diffuse.2. Migration of polymorphonuclear leukocytes was not found. Demarcation shaft is not generated.
5 days1. The infarction area presents nekrotizirovannye cardiomyocytes, surrounded demarcation shaft.1. The infarction area presents a deathly modified cardiomyocytes phenomena is of plasmolysis, plasmolysis and karyolysis.
2. Signs of the formation of granulation tissue.2. On the periphery of the perifocal region detected accumulations of lymphocytes and macrophages, there is a proliferation of fibroblasts, i.e. elements of granulation tissue.
3. In adjacent structures marked neutrophilic infiltration Indonesia.
7 days1. Saved disintegration of muscle cells.1. The infarction area presented by granulation tissue of proliferating fibroblasts and macrophages.
2. On the edges of the zone of necrosis is formed granulation tissue with a large number of fibroblasts, sinusoidal emocapella.2. In the area of the scar is determined moderate lymphocytic infiltration, macrophages and proliferating fibroblasts.
3. Saved infiltration by lymphocytes and segmented by leukocytes.

The principal difference histomorphologically pictures of animals with experimental myocardial infarction, polucavsie the different chemical structure of the immunomodulators and not receiving treatment, revealed in the presence of non-treated animals expressed leukocyte inflammation in the area of heart attack, which led to an increase in the spread of inflammation on the original intact myocardium and much later scarring of the myocardium. In animals with experimental myocardial infarction treated with immunomodulators, such as tumeric, the drug caused the predominance leviitra-macrophage inflammatory reaction, uskoreva regenerative processes in the zone of necrosis and colonrectum areas. Almost the same effectiveness of the treatment and, most importantly, the same histomorphologically picture in the area of inflammation suggests that different chemical structure immunomodulators have the same mechanism of action and provide equally effective therapeutic effect in acute myocardial infarction.

Method of treatment with immunomodulators myocardial infarction in rats after simulation-based medical intervention when creating a model of myocardial infarction is intravenous immunocorrector Tamarit in the dosage of 3 mg/kg every day for seven days with histological studies of myocardial tissue after the first, third and seventh days, and the results of these studies, the people on the adequacy and effectiveness of the treatment.



 

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SUBSTANCE: modelling a myocardial infraction is followed in a rat is followed by intravenous introduction of the immune corrector tamerite 3 mg/kg. The preparation is injected daily for seven days. The histological results of the myocardial tissue presented after the first, third and seventh days show the sufficiency and efficacy of the therapy.

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