Mulch J, Schaper J, Gottwik M, Hehrlein F W
Thorac Cardiovasc Surg. 1979 Jun;27(3):145-52. doi: 10.1055/s-0028-1096235.
Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was also a disturbance in the autoregulative mechanisms of coronary perfusion and an uncoupling of O2-consumption and mechanical efficiency. A prolonged reperfusion period of the heart beating empty allowed ultrastructural recovery of the damaged myocardium. In contrast, functional recovery of the myocardium, as determined by several parameters of contraction and relaxation, did not correlate with ultrastructural recovery and was not improved by prolonged reperfusion.
在离体心脏模型中，研究了正常体温下缺血期间犬心肌的收缩和舒张情况。张力发展的降低取决于缺血持续时间。尽管再灌注时间超过1小时，但缺血时间超过30分钟后，观察到功能恢复不足。缺氧期间观察到顺应性降低，但仅在缺血60分钟后才出现持续性舒张缺陷。在此期间后，冠状动脉灌注的自动调节机制也出现紊乱，耗氧量与机械效率解偶联。心脏空跳状态下延长再灌注时间可使受损心肌的超微结构恢复。相比之下，由收缩和舒张的几个参数所确定的心肌功能恢复与超微结构恢复无关，且延长再灌注并不能改善。
