Mechanisms of Parasympathetic Influences on the Heart in the Development of of the Effect Antiischemic Distant Conditioning Myocardium

The aim of the study: to investigate the involvement of distinct parasympathetic and sympathetic beta-adrenergic mechanisms in infarct-limiting effect of remote ischemic conditioning. Materials and methods. Experiments have been conducted on white male rats. Remote ischemic conditioning was performed as 15-min bilateral femoral arteries occlusion before the onset of myocardial ischemia (RIPC, n=8), on the 10-th minute of ischemia (RIPerC, n=8) or on the 10-th minute of reperfusion (RIPostC10', n=8). To study the role of vagal nerves in the development of remote ischemic conditioning femoral arteries occlusion was performed in conditions of bilateral vagotomy (Vagotomy+RIPC, n=8; Vagotomy+RIPerC, n=7; Vagotomy+RIPostC10', n=8). M-cholinoreceptors were blocked by atropine (groups Atropine+RIPC, n=10; and Atropine+RIPostC10', n=6). Beta-adrenoreceptors blockade was induced by injection of metoprolol or atenolol on the 1-st minute of reperfusion to animals with intact vagal nerves (groups MetR+RIPostC10', n=10; and AtenR+RIPostC10', n=10) or after bilateral vagotomy (groups Vagotomy+MetR+RIPostC10', n=10; Vagotomy+AtenR+RIPostC10', n=10). Results. RIPC, RIPerC и RIPostC10' limited infarct size by 56%, 58% and 49% respectively (all p 0,05 vs Control, p<0,001% vs RIPostC10'). Conclusions. Cardioprotective effect of RIPC and RIPerC is mediated mainly by vagal control of heart, whereas in RIPostC10' beta-adrenoreceptors are also important. Meanwhile, М-cholynoreceptors stimulation is a key point in the development of both RIPC, as well as RIPostC10'.