Carbonin P, Di Gennaro M, Valle R, Beranbei R, Habed A
Am J Physiol. 1980 Sep;239(3):H380-90. doi: 10.1152/ajpheart.1980.239.3.H380.
The electrogram (EG) of the isolated rat heart during ischemic or anoxic perfusion has been studied. Reduction of the coronary flow rate (CFR) induced an increase of voltage (V) both in unipolar epicardial EG and in transmural bipolar EG. The V increase did not occur during anoxic perfusin. The ischemic increase cannot be due to a disturbance in the His-Purkinje or intraventricular conduction because it was observed also in the circumscribed myocardial area, which was explored by means of the transmural bipolar EG. Likewise it cannot be due to an intramural block because it occurs before one observes an augmentation of epicardial activation time or a decrease of dV/dtmax. Therefore, the ischemic V increase should be due to a modification of transmembrane potential. The variation rate of V, of dP/dt, and of myocardial ATP behaved in a similar way during underperfusion. Varying intracellular Ca2+ by means of a Ca2+-free medium or verapamil reduces the ischemic V increase. The dynamics of the ischemic V increase may be represented in order of succession by: inhibition of oxidative metabolism, augmentation of intracellular Ca2+, increase of K+ conductance, and hyperpolarization of cardiac cells.
对离体大鼠心脏在缺血或缺氧灌注期间的心电图(EG)进行了研究。冠状动脉血流速率(CFR)降低会导致单极心外膜EG和透壁双极EG的电压(V)升高。在缺氧灌注期间未出现V升高。缺血性升高并非由于希氏-浦肯野系统或心室内传导紊乱所致,因为在通过透壁双极EG探测的局限性心肌区域也观察到了这种情况。同样,它也不是由于壁内阻滞所致,因为它发生在观察到心外膜激活时间延长或dV/dtmax降低之前。因此,缺血性V升高应归因于跨膜电位的改变。在灌注不足期间,V、dP/dt和心肌ATP的变化率表现相似。通过无钙培养基或维拉帕米改变细胞内Ca2+会降低缺血性V升高。缺血性V升高的动态过程依次表现为:氧化代谢抑制、细胞内Ca2+增加、K+电导增加和心肌细胞超极化。