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Biomedical subjects

A N Kudrin

Publications and source records attributed to A N Kudrin.

At least 19 recordsLinked to original sources
PubMed1992

The mechanisms of free-radical lipids and antioxidant heart protection in experimental ischaemia and infarction.

Free-radical lipid peroxidation (FRLP) during experimental myocardial ischaemia and infarction was studied on the first author's model using coronary occlusion in more than 1500 albino rats. FRLP was tested at various intervals after coronary occlusion (from the 20th minute to 14--30 days) in myocardial lipid extracts using various methods: 1) chemiluminescent method determining the intensity of free radical reactions, 2) diene conjugate production, 3) malone dialdehyde reaction, 4) Schiff bases fluorometric determination. The severity of ischaemia and infarction was assessed according to electrocardiographic, light and electron microscopic findings and morphometry of the damaged area. Intensified FRLP was registered in all four indicators at most tests performed within the first 14 days after production of ischaemia and infarction. The severity of ischaemic lesion could be reduced by FRLP inhibition using antioxidative agents of sharply differing chemical nature (sodium selenite, alpha-tocopherol a.o.). The authors conclude that FRLP intensification plays a role in the pathogenesis of myocardial ischaemia and infarction, and recommend to include antioxidative drugs in comprehensive heart protection.

Animals↗
PubMed1986

[Formation of the marginal "pro-oxidant" zone and its role in the enhancement of lipid peroxidation in the area of myocardial ischemia and infarction].

The formation of peripheral zone devoid of dehydrogenase activity but possessing vessels connected with the normal myocardium was demonstrated in the area of fresh myocardial infarction 2 h after coronary occlusion. A direct correlation between the changes of the zone area and the intensity of free radical lipid peroxidation in the area of fresh myocardial infarction was established.

Animals↗
PubMed1986

[Characteristics of the "no-reflow" phenomenon in reperfusion of the myocardium depending upon the duration of ischemia].

The dynamics of changing dimensions of "no reflow" area following reperfusion after 30 min-1 h-long ischemia is characterized by three basic phases. The reperfusion following and hour-long ischemia altered considerably the character of phases of "no reflow" phenomenon. The data obtained suggest that the therapy of transitory ischemia must be directed not only to ischemia itself, but also to postischemia reperfusion-induced "no reflow" phenomenon.

Animals↗
PubMed1984

[Limited area of coronary-occlusion myocardial infarct in rats undergoing antioxidant therapy].

The synthetic antioxidant dibunol, (ionol. 2,6-ditret-butyl-4-methylphenol) produces the limitation of the zone of the coronaro-occlusion myocardial infarction in rats by 15.8 and 24.2% on day 7 during daily oral administration in doses of 80 and 120 mg/kg, respectively. In the doses used, dibunol reduces the activity of glutathione peroxidase but does not change the activity of glutathione-S-transferase and superoxide dismutase in the infarction zone of the myocardium. It is concluded that free radical products play an important role in ischemic and infarction damage to the myocardium.

Animals↗
PubMed1984

[Changes in the activity of antioxidant enzymes in ischemia and subsequent reperfusion of the myocardium].

Transitory coronary failure of the myocardium was accompanied by a considerable reduction in the activity of superoxide dismutase, glutathione peroxidase and glutathione transferase, with the activity of the enzymes under study being not different in the ischemized and distant from ischemia zones of the myocardium. Reperfusion did influence the activity of superoxide dismutase and glutathione peroxidase after 10 and 40 minutes of ischemia, whereas following 120 minutes of ischemia the activity of superoxide dismutase ascended after 10 and 40 minutes of reperfusion while the activity of glutathione peroxidase remained unchanged.

Animals↗
PubMed1984

[Effect of the beta-adrenoblockader atenolol on the extent of myocardial necrosis in transient and permanent coronary occlusion].

It has been demonstrated in experiments on rats that atenolol in a dose of 10 mg/kg exerts an antiischemic action in transitory coronary occlusion lasting 30 minutes followed by reperfusion for 23h and 30 min. The effect manifested in the diminution of the relative area and mass of myocardial necrosis zone and in the dilatation of the left ventricle. Atenolol also produced an antiischemic action in permanent coronary occlusion for 24 h. However, the effect in the latter case was less marked than in transitory occlusion. When injected for permanent occlusion, atenolol (10 mg/kg i. v.) led to a 1.59-fold decrease in the necrosis area and a 2.1-fold decrease (p less than 0.001) when administered for transitory occlusion. The mass of the myocardial necrosis zone also dropped (by 1.65-fold and 2.3-fold, respectively), whereas the degree of dilatation by 2.1- and 2.3-fold, respectively.

Animals↗
PubMed1984

[Changes in the size of the myocardial damaged area in postischemic reperfusion].

The changes in the size of the myocardial injury area during reperfusion after the coronary occlusion-induced ischemia lasting 30 minutes are phasic in nature. Until 3.5 h the injured area increases and after 23.5 h relatively diminishes. After a more prolonged ischemia such manifestations are either unmarked or absent. Ischemia lasting from 30 min to 4 hours followed by reperfusion, as compared with ischemia of the same duration without reperfusion, normally gives rise to the formation of an area of injury, which is less or occasionally equal in size. The data obtained and reported indicate that in the area of coronary occlusion there are groups of cardiomyocytes that differ as regards the resistance to ischemia.

Animals↗
PubMed1983

[Alcohol and drugs].

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Alcoholic Intoxication↗