Vogel W M, Briggs L L, Apstein C S
J Mol Cell Cardiol. 1985 Jan;17(1):57-70. doi: 10.1016/s0022-2828(85)80092-4.
Ischemic myocardial contracture is exacerbated by reperfusion. This study examines the extent to which intensification of contracture by reperfusion is due to metabolic reoxygenation phenomena or hydraulic erectile contributions of coronary perfusion to left ventricular (LV) stiffness. Isolated rabbit hearts, with fluid-filled LV intraventricular baloons, were subjected either to: control aerobic perfusion; 30 or 60 min of global ischemia; 60 min of hypoxia with constant coronary flow; or 10 min of calcium-free perfusion to cause calcium paradox injury. During reperfusion with control perfusate isovolumic LV end diastolic pressure (LVEDP) was measured with constant coronary flow and during transient, 1 min, total global ischemia to measure the contribution of the coronary perfusion to LVEDP. In all injured groups LVEDP was increased compared to control hearts. The decrease in LVEDP during transient ischemia was greater in damaged hearts than in controls, demonstrating a greater contribution of coronary perfusion to LVEDP after injury. Only in the hypoxic hearts did diastolic fiber tension increase upon reperfusion. Inherent diastolic fiber tension decreased during 15 to 60 min of reperfusion in the ischemic and hypoxic injury groups, a trend which was masked by an increasing effect of coronary perfusion on LV chamber stiffness. During the reperfusion period enhancement of the erectile effect was more pronounced at higher preloads. Thus, reperfusion contracture was maintained both by changes in inherent fiber stiffness and by changes in the erectile effect. These contributions changed over time and varied with the type and severity of injury, but after all types of injury the erectile vascular effect made a greater contribution to diastolic chamber stiffness than inherent fiber tension.
缺血性心肌挛缩会因再灌注而加剧。本研究探讨了再灌注导致挛缩加剧的程度是由于代谢性复氧现象，还是冠状动脉灌注对左心室（LV）僵硬度的液压勃起作用。将装有液体的左心室内球囊的离体兔心分别进行以下处理：对照有氧灌注；30或60分钟的全心缺血；60分钟恒定冠状动脉血流的缺氧；或10分钟无钙灌注以引起钙反常损伤。在使用对照灌注液进行再灌注期间，以恒定冠状动脉血流测量左心室等容舒张末期压力（LVEDP），并在短暂的1分钟全心缺血期间测量冠状动脉灌注对LVEDP的贡献。与对照心脏相比，所有损伤组的LVEDP均升高。受损心脏在短暂缺血期间LVEDP的下降幅度大于对照组，表明损伤后冠状动脉灌注对LVEDP的贡献更大。只有在缺氧心脏中，再灌注时舒张期纤维张力才会增加。在缺血和缺氧损伤组中，再灌注15至60分钟期间固有舒张期纤维张力下降，这一趋势被冠状动脉灌注对左心室腔僵硬度的增强作用所掩盖。在再灌注期间，较高预负荷时勃起效应的增强更为明显。因此，再灌注挛缩是由固有纤维僵硬度的变化和勃起效应的变化共同维持的。这些贡献随时间变化，并因损伤的类型和严重程度而异，但在所有类型的损伤后，勃起血管效应对舒张期腔僵硬度的贡献均大于固有纤维张力。
