[Electrophysiologic study of the anti-arrhythmic mechanism of action of phosphocreatine in acute myocardial ischemia and reperfusion]. / Elektrofiziologicheskoe issledovanie mekhanizmov antiaritmicheskogo deistviia fosfokreatina pri ostroi ishemii i reperfuzii miokarda.

To determine the possible application of exogenous phosphocreatine (ePC) to protect the ischemic myocardium from reperfusion abnormalities in cardiac rhythm, the antiarrhythmic and antifibrillatory activities of the agent were studied in an acute myocardial ischemia model and reperfusion-induced cardiac damage. It was shown that ePC produced a pronounced antifibrillatory effect in acute coronary occlusion and subsequent reperfusion. The agent substantially increased the threshold of electric ventricular fibrillation and the frequency of spontaneous defibrillation. The highest activity was shown by ePC in ischemic myocardial reperfusion. The agent suppressed both rapid inward Na+ current and slow inward Ca2+ current. The effects of ePC on transmembrane ion currents suggest that the agent has a unique electrophysiological mechanism of action involving the properties of Classes I and IV antiarrhythmics, making ePC promising in clinical application in patients with impaired conduction and automatism.

[Prospects for correcting the disrupted status of the cardiovascular system in acute myocardial ischemia by combined experimental use of phosphocreatine and corinfar]. / Izuchenie vozmozhnosti korrektsii narushenii sostoianiia serdechno- sosudistoi sistemy pri ostroi ishemii miokarda putem sochetannogo primeneniia fosfokreatina i korinfara v éksperimente.

Individual and simultaneous influence of phosphocreatine and calcium antagonist corinfar on hemodynamics patterns was studied in experimental acute ischemia of myocardium. Simultaneous treatment with phosphocreatine and corinfar may be effective in ischemic impairment of myocardium.

[Study of anti-ischemic action of carnitine chloride and its effects on the effectiveness of antianginal agents]. / Issledovanie protivoishemicheskogo deistviia karnitina khlorida i ego vliianiia na éffektivnost' antianginal'nykh sredstv.

The experiments with models of myocardial infarction established that carnitine chloride reduced the size of an ischemic zone, prevented oxidative metabolism, lowered ATP and creatine phosphate levels, inhibited lactate and free fatty acid accumulation in the ischemic myocardium. Carnitine chloride in combination with nitrong and isoptin increased the anti-ischemic potency of the former.