Regan T J, Passannante A J, Khan M I, Oldewurtel H A, Jesrani M U
J Clin Invest. 1971 Mar;50(3):534-42. doi: 10.1172/JCI106522.
Obstruction of a major branch of the left coronary artery in a previously normal ventricle is not usually associated with shock, experimentally or clinically. To examine the early hemodynamic alterations which may determine the course of ischemia when myocardial scar exists from previous infarction, 16 animals were successfully studied 9 wk after obstruction of the left circumflex artery. Acute ischemia during thrombus formation in the anterior descending artery of intact anesthetized dogs with scar was compared with animals undergoing the same procedure in the absence of scar (group 1). In the chronic animals, two types of hemodynamic responses were observed. Group 2 was characterized by heart failure usually persisting through 3 hr, and group 3 by a different ventricular volume response and rapidly developing shock. The weight of ischemic and scar areas were comparable and coronary blood flow ((85)Kr method) to the ischemic site was reduced to a similar extent. Animals in groups 1 and 2 remained normotensive and had similar elevations of left ventricular enddiastolic volume (indicator dilution method) during the initial 60 min of ischemia. Group 2 had a significantly larger rise of end-diastolic pressure, presumably related to altered elastic properties associated with scar of subendocardial distribution. Group 3 had a stroke volume decline that was not significantly greater than group 2 and both groups had an initial rise of peripheral vascular resistance. Despite a nearly fourfold increase of left ventricular end-diastolic pressure, there was a significant decline of left ventricular end-diastolic volume in group 3. This preceded the onset of hypotension in group 3, with arterial pressure declining to a greater extent than stroke volume, usually culminating in cardiac standstill. Group 3 was distinguished by the presence of transmural scar, which was postulated to influence contiguous ischemic tissue in diastole so as to diminish ventricular volume. By analogy with the hemodynamics of acute pericardial tamponade, a reflex pathway activated in the myocardium in response to reduced end-diastolic volume has been suggested as a mechanism for the arterial hypotension.
在先前正常的心室中，左冠状动脉主要分支的阻塞在实验或临床上通常不会导致休克。为了研究当存在既往梗死形成的心肌瘢痕时，可能决定缺血进程的早期血流动力学改变，在左旋支动脉阻塞9周后，对16只动物进行了成功研究。将有瘢痕的完整麻醉犬在前降支动脉血栓形成期间的急性缺血与无瘢痕的相同手术动物（第1组）进行比较。在慢性动物中，观察到两种血流动力学反应。第2组的特征是心力衰竭通常持续3小时，第3组则表现为不同的心室容积反应并迅速发展为休克。缺血区和瘢痕区的重量相当，缺血部位的冠状动脉血流（（85）Kr法）减少程度相似。第1组和第2组动物在缺血最初60分钟内血压正常，左心室舒张末期容积（指示剂稀释法）有相似程度的升高。第2组舒张末期压力升高明显更大，可能与心内膜下分布的瘢痕相关的弹性特性改变有关。第3组的每搏输出量下降幅度并不比第2组显著更大，两组外周血管阻力均有初始升高。尽管第3组左心室舒张末期压力几乎增加了四倍，但左心室舒张末期容积却显著下降。这先于第3组低血压的发生，动脉压下降幅度大于每搏输出量，通常最终导致心脏停搏。第3组的特征是存在透壁性瘢痕，推测其在舒张期影响相邻的缺血组织，从而减小心室容积。类似于急性心包填塞的血流动力学情况，有人提出心肌中因舒张末期容积减少而激活的反射通路是动脉低血压的一种机制。
