РОЛЬ СИМПАТОАДРЕНАЛОВОЙ СИСТЕМЫ В ИШЕМИЧЕСКОМ ПРЕКОНДИЦИОНИРОВАНИИ СЕРДЦА

Data on the role of catecholamines in the ischemic preconditioning (IPre) is controversial. The authors of a number of studies found no effect of IPre at the level of norepinephrine in the myocardium or norepinephrine entry in the coronary effluent. Other researchers have noted the rise of the interstitial norepinephrine level or release of this neurotransmitter in the myocardium in response to IPre. в-Adrenoceptors (AR) do not participate in the infarct-limiting effect of IPre but are involved in the inotropic effect of preconditioning. It was established that the cardioprotective effect of IPre is associated with activation of the б1-AR. According to some authors, the depletion of the store of endogenous catecholamines leads to the disappearance of the cardioprotective effect of IPre and the other results say that the protective effect of preconditioning saved after reducing the amount of stored catecholamines. Mobilization of endogenous catecholamines before coronary occlusion increases heart resistance to the pathogenic impact of ischemia and reperfusion. Stimulation of the б1-AR mimics the cardioprotective effect of IPre. The cardioprotective effect of б1-agonists is mediated through Gi/o-proteins and is linked to protein kinase C activation and opening mitoKATP channels. It is found that preliminary в-AR stimulation enhances tolerance of heart to ischemia reperfusion. Molecular mechanism of cardioprotective action of в-AR stimulation is different from the signaling mechanism of IPre.