[Molecular mechanisms of hypoxia and adaptation to it. Part II].

Reprogramming of the mitochondrial electron transport chain (ETC) is the most important physiological mechanism that provides short- and long-term adaptation to hypoxia. The possibilities of additional pharmacological regulation of ETC activity are of considerable practical interest in correcting hypoxia-associated disorders. This review considers the main groups of antihypoxic compounds that exhibit their effect at the interface of ETC and the cycle of tricarboxylic acids, including succinate-containing and succinate-forming antihypoxants.

[Molecular mechanisms for hypoxia development and adaptation to it. Part I].

Hypoxia is a typical pathological process characterized by the occurrence of oxygen deficiency in tissues and cells and accompanied by the development of immediate and delayed compensatory and adaptive reactions. Reprogramming of the mitochondrial electron transport chain (ETC) function is one the most essential regulatory mechanisms that allow for immediate adaptation to hypoxia. Succinic acid, or succinate, is involved in this process not only as one of the intermediates of the tricarboxylic acid (TAC) cycle, but also as a signaling molecule.

[The effect of uridine and uridine nucleotides on isolated rat heart performance in regional myocardial ischemia].

We studied the effects of uridine, uridine-5'-monophosphate (UMP), uridine-5'-diphosphate (UDP) and uridine-5'-triphosphate on contractility, coronary flow and heart rate in isolated perfused rat hearts under 60-minute regional ischemia of the left ventricle. All the compounds (50 mumol/l) induced a positive inotropic effect but had no effect on the heart rate. Uridine and UMP prevented the development of the contracture.

[The role of the muscarinic, adenosine and adrenoreceptors of the heart in the development of postischemic reperfusion ventricular fibrillation].

The authors studied the effect of m-cholino-, adreno-, and purinotropic agents on the development of postischemic reperfusion fibrillation of isolated rat hearts. Pilocarpine, norepinephrine, phenylephrine, and adenosine caused a proarrhythmogenic effect. Atropine, trimedoxim, prazosin, and chloroquine made fibrillation less expressed.

[Effect of purine nucleosides on the contractile function of the rat heart in ischemia and reperfusion].

The Langendorf isolated rat hearts underwent 30-minute total ischemia followed by 60-minute reperfusion. Adenosine, inosine or guanosine was added at a concentration of 50 mumol/l into the perfusate in the first 30 minutes. The nucleotides significantly increased the developed pressure and the maximum left ventricular contractility rate.

[The effect of adenosine on the contractile function of the heart during experimental ischemia and reperfusion].

It has been shown that 30 min ischemia followed by 30 min reperfusion inhibits cardiac contractility. The addition of adenosine at a concentration of 50 or 100 mumol/l into the perfusate normalized a decreased cardiac contractility and prevented the onset of contracture.

[Hemodynamic effects of purine nucleosides in regional ischemia and reperfusion].

The rat hearts were subjected to 60-min ischemia by left coronary artery ligation followed by 60-min reperfusion, involving intravenous adenosine inosine or guanosine given in a dose of 1 mg/kg.min-1 in the first 30 minutes of reperfusion. Ischemia and subsequent reperfusion caused a progressive decrease in cardiac output and coronary blood flow.