Meerson F Z
Laboratory of Hearth Pathophysiology, USSR Academy of Medical Sciences, Moscow.
J Mol Cell Cardiol. 1989 Mar;21(3):299-303. doi: 10.1016/0022-2828(89)90745-1.
Adaptation to repeated stress prevents or limits ischemic and reperfusion arrhythmias in the whole organism. In studying mechanism of this phenomenon, we have investigated the effect of local ischemia and subsequent reperfusion on the function of isolated hearts of rats adapted to the stress of repeated immobilization. We established that such adaptation limited the depression of the amplitude and velocity of contraction and velocity of relaxation of the heart in ischemia and subsequent reperfusion. Simultaneously this adaptation limited reperfusion-induced arrhythmias to a considerable extent; in particular, the duration of reperfusion-induced fibrillation was reduced two-fold. Thus the cardioprotective antiarrhythmic effect of adaptation of the organism to stress exposure depends not only on adaptive alterations of central regulation, but to a considerable extent, is determined by processes occurring at the level of the heart itself.
对反复应激的适应可预防或限制整个机体的缺血及再灌注心律失常。在研究这一现象的机制时,我们研究了局部缺血及随后的再灌注对适应反复固定应激的大鼠离体心脏功能的影响。我们发现,这种适应限制了缺血及随后再灌注时心脏收缩幅度、收缩速度和舒张速度的降低。同时,这种适应在很大程度上限制了再灌注诱导的心律失常;特别是,再灌注诱导的颤动持续时间缩短了一半。因此,机体对应激暴露的适应所产生的心脏保护抗心律失常作用不仅取决于中枢调节的适应性改变,而且在很大程度上取决于心脏本身水平上发生的过程。