BIOCHEMICAL CHANGES IN ISOLATED PERFUSED HEARTS

Langendorff悬挂心脏制备物（离体、灌注、功能性大鼠 心脏）已被证明在以下条件下会遭受功能损伤 缺血 对心脏进行了各种治疗， 在这种缺血期间的功能损伤。为了评估 在这些缺血期间发生的生化变化，心脏 组织已被提取，提取物已被检查的酶 活性和羰基含量。缺氧条件， 严重到只能提供50%的功能恢复，原因 肌酸激酶（CPK）活性变化不大，无论是在 缺氧期间或随后的再灌注期间。 与此同时， 而乳酸脱氢酶活性在缺氧和复氧过程中升高， 再灌注时的初始值。 羰基含量，一种衡量 氧化损伤，在缺氧期间经历适度增加， 在再灌注时，这与自由基的概念一致， 自由基的产生和相关的氧化发生在重新引入时 在缺氧期间，有一种 ATP明显丧失，同时AMP及其分解产物增加， 次黄嘌呤和黄嘌呤。 再灌注后，ATP水平上升 接近初始值和AMP、黄嘌呤和次黄嘌呤水平 回到原来的低水平。 有趣的是，ADP水平变化非常大， 在缺血或再灌注期间很少。

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 anoxia, which are serious enough to provide only a 50 percent recovery of function, cause little change in the creatine kinase (CPK) activity, whether during the period of anoxia or during subsequent reperfusion. At the same time, however, lactate dehydrogenase activities rise during the anoxia and return to initial values upon reperfusion. Carbonyl content, a measure of oxidative damage, undergoes a modest increase during anoxia 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 anoxic tissue, During the period of anoxia, 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.