This investigation in devoted to the study of metabolite tropic mechanisms of cardioprotective activity of new original antianginal and antihypertensive drug Hypertril, derivative of 4-amino-1,2,4-triazole. Parenteral introduction of Hypertril in 2.5 mg/kg dose shows pronounced cardioprotective and antiischemic effect on occlusive and izadrine-pituitrin models of myocardial infarction. As opposed to Metoprolol, Hypertril shows significant cardioprotective effect by 45 minutes earlier in acute myocardial ischemia. Hypertril inhibits mitochondrial pore opening and increase of charge of inner membrane of cardiomyocites mitochondria, it increases the level of ATP and ADP against the background of growing malate and pyruvate levels, activity of NAD-malate dehydrogenase and decrease of lactate in myocardium. Important features of cardioprotective effect of Hypertril are decrease of mitochondrial dysfunction manifestations in myocardial ischemia and increase of myocardium energy-supply by activation of compensatory cytosolic-mitochondrial energy pathway. All above-said is considered to be experimental justification of further study of potential preparation Hypertril with the aim of clinical application as antianginal drug.
