Dolgikh V T
Anesteziol Reanimatol. 1989 May-Jun(3):51-6.
The investigation has been performed on the isolated isovolumically contracting hearts of rats resuscitated after a 4-min clinical death caused by acute blood loss. It has been established that myocardial contractility disturbances, minimum during clinical death, become far more marked 30-60 min after recirculation and progress in the first 3 days, especially in unfavourable course of the postresuscitation period. Disturbed myocardial contractility closely correlates with enzyme release into the coronary flow and the efficacy of glucose utilization per unit of myocardial function. By day 7 contractility disturbances attenuate, mounting again two weeks later. Relative normalization of myocardial contractility is observed by the end of the first postresuscitation month, however, the release of enzymes from various cardiomyocyte ultrastructures into the coronary flow remains still high.
对因急性失血导致4分钟临床死亡后复苏的大鼠离体等容收缩心脏进行了研究。已确定，心肌收缩力紊乱在临床死亡期间最小，在再灌注后30 - 60分钟变得更加明显，并在最初3天内进展，尤其是在复苏后时期的不利病程中。心肌收缩力紊乱与酶释放到冠状动脉血流中以及单位心肌功能的葡萄糖利用效率密切相关。到第7天时，收缩力紊乱减弱，两周后再次加剧。在复苏后第一个月末观察到心肌收缩力相对正常化，然而，各种心肌细胞超微结构中的酶释放到冠状动脉血流中仍然很高。
