Ventricular contracture and compliance changes with global ischemia and reperfusion, and their effect on coronary resistance in the rat.
Ventricular contracture and compliance changes with global ischemia and reperfusion, and their effect on coronary resistance in the rat.
复制标题
心室挛缩和顺应性随整体缺血和再灌注的变化，及其对大鼠冠状动脉阻力的影响。
DOI：
10.1161/01.res.41.2.206
复制
发表时间：
1977
影响因子：
20.1
通讯作者：
W. Hood
中科院分区：
文献类型：
--
作者：
C. Apstein;M. Mueller;W. Hood
我们测量了大鼠离体心脏在全脑缺血30分钟期间和之后的心室收缩和顺应性（被动扩张性）。在对照、缺血和再灌注期间，左心室内压与容积的被动充盈或扩张性曲线在0和30 mm Hg之间呈线性。缺血时心室的有效刚度（扩张性斜率）从缺血前的0.229 ± 0.027增加到0.514 ± 0.083 mm Hg/pl（P < 0.005），再灌注时刚度显著增加到1.743 ± 0.442 mm Hg/pl（P < 0.001）。被动扩张性的变化与心室保持在等容状态时发生的挛缩变化平行;在缺血期间，挛缩使缺血前舒张压增加-2 ± 1至17 ± 3 mm Hg在再灌注早期，当压力为75 ± 6 mm Hg时，心室发生强烈挛缩（与缺血前对照组相比，P < 0.001）。再灌注30分钟后，挛缩压力降至34 ± 7 mm Hg（与对照组相比P < 0.001）。再灌注过程中的挛缩与冠状动脉血管阻力的平行增加有关;因此，缺血后挛缩可能导致缺血心肌尝试再灌注时观察到的无复流现象。缺血和再灌注过程中发生的挛缩的严重程度与缺血组织乳酸积累量呈负相关，与组织含水量的变化无关。因此，全脑缺血和再灌注明显降低了心室的被动顺应性;在完整的动物中，心室充盈可能会受到这一过程的损害，舒张压测量也会反映顺应性的变化。
SUMMARY We measured ventricular contracture and compliance (passive distensibility) of the isolated rat heart during and after 30 minutes of complete global ischemia. The passive filling or distensibility curves of intra-left ventricular pressure vs. volume were linear between 0 and 30 mm Hg during the control, ischemic, and reperfusion periods. During ischemia the effective stiffness (distensibility slope) of the ventricle increased from the preischemic control of 0.229 ± 0.027 to 0.514 ± 0.083 mm Hg/pl (P < 0.005); with reperfusion, stiffness markedly increased to 1.743 ± 0.442 mm Hg//tl (P < 0.001 vs. control). The changes in passive distensibility were parallel to changes in contracture which occurred when the ventricle was held in the isovolumic condition; during ischemia, contracture increased the preischemic diastolic pressure of -2 ± 1 to 17 ± 3 mm Hg (P < 0.001); in the early reperfusion period intense ventricular contracture occurred to a pressure of 75 ± 6 mm Hg (P < 0.001 vs. preischemic control). After 30 minutes of reperfusion contracture pressure decreased to 34 ± 7 mm Hg, (P < 0.001 vs. control). Contracture during reperfusion was associated with a parallel increase in the coronary vascular resistance; postischemic contracture may thus contribute to the no reflow phenomenon observed with attempted reperfusion of ischemic myocardium. The severity of contracture which occurred during ischemia and reperfusion was inversely related to the amount of ischemic tissue lactate accumulation and did not correlate with changes in tissue water content. Thus, global ischemia and reperfusion markedly decreased passive ventricular compliance; in the intact animal ventricular filling could be impaired by this process and diastolic pressure measurements would reflect the change in compliance as well in