BIOCHEMICAL CHANGES IN ISOLATED PERFUSED HEARTS

兰根多夫悬挂心脏制剂(隔离、灌流、起作用 大鼠心脏)已被证明在条件下会受到功能损害 脑缺血的症状。对心脏进行了各种治疗，以 最大限度地减少在这种缺血期的功能损害。为了 评估在这些缺血期发生的生化变化， 心脏组织已经被提取，并对提取物进行了检查 用于酶活性和羰基含量。缺血状态 其严重程度仅能提供50%的恢复 功能，对肌酸激酶(CPK)或异柠檬酸的影响很小 脱氢酶活性，无论是在缺血期还是在 随后的再灌流。然而，与此同时，乳酸脱氢酶 活动在缺血过程中升高，并在 再灌流和谷草转氨酶活性升高 在缺血期间有所下降。羰基含量，一种衡量 氧化损伤在缺血期间略有增加，但增加 在再灌流时戏剧性地，与自由的想法一致 自由基的产生和相关的氧化在重新引入时发生 向缺血组织输送氧气。在缺血期，有 伴随AMP升高的ATP显著丧失及其崩溃 产品，肌苷，次黄嘌呤和黄嘌呤。在再灌流时，ATP 水平上升到接近初始值，AMP、黄嘌呤和次黄嘌呤 水平恢复到原来的低水平。有趣的是，ADP水平 在缺血或再灌注期变化很小。那里 脑缺血时同工酶的分布是否没有明显的变化 肌酸激酶，但乳酸脱氢酶表现出一定的移位 从心脏相关的、更需氧的单体到肝脏相关的， 有氧单体较少。在再灌流时，单体的分布 回到缺血前的状态。

Langendorff hanging heart preparations (isolated, perfused, functioning rat hearts) have been shown to suffer functional damage under conditions of ischemia. Various treatments have been imposed upon the hearts to minimize the functional damage during such ischemic periods. In order to assess the biochemical changes occurring during these ischemic periods, the heart tissue has been extracted and the extracts have been examined for enzymic activities and for carbonyl content. Conditions of ischemia which are serious enough to provide only a 50 percent recovery of function, cause little change in creatine kinase (CPK) or isocitrate dehydrogenase activities, whether during the period of ischemia or during subsequent reperfusion. At the same time, however, lactate dehydrogenase activities rise during the ischemia and return to initial values upon reperfusion and glutamate-oxalacetate transaminase activities rise somewhat and then drop during ischemia. Carbonyl content, a measure of oxidative damage, undergoes a modest increase during ischemia but rises dramatically upon reperfusion, consistent with the idea that the free radical production and associated oxidation occurs upon the reintroduction of oxygen to the ischemic tissue. During the period of ischemia, there is a marked loss of ATP accompanied by rises in AMP and its breakdown products, inosine, hypoxanthine, and xanthine. Upon reperfusion, the ATP levels rise to near initial values and the AMP, xanthine, and hypoxanthine levels return to their original low levels. Interestingly, ADP levels change very little during the periods of ischemia or reperfusion. There are no apparent ischemia-dependent changes in isozyme distribution for creatine kinase, but lactate dehydrogenase demonstrates a definite shift from the heart-associated, more aerobic monomers to the liver-associated, less aerobic monomers. Upon reperfusion, the distribution of the monomers returns to that seen prior to ischemia.