Prolonged abnormalities of myocardium salvaged by reperfusion.
Prolonged abnormalities of myocardium salvaged by reperfusion.
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通过再灌注挽救心肌的长期异常。
DOI：
10.1152/ajpheart.1981.241.4.h591
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Braunwald,E
中科院分区：
文献类型：
--
作者：
Kloner,RA;DeBoer,LW;Darsee,JR;Ingwall,JS;Hale,S;Tumas,J;Braunwald,E
本研究的目的是确定通过冠状动脉再灌注挽救的非坏死缺血后心肌中是否持续存在生化、功能和超微结构异常。麻醉狗的左冠状动脉前降支 (LAD) 闭塞 15 分钟，然后再灌注 3 天。获得活组织检查以测量腺苷 5'-三磷酸 (ATP) 和磷酸肌酸 (CP) (nmol/mg 蛋白质)，并使用声测法评估区域功能。闭塞 15 分钟后，非缺血心内膜下心肌 ATP 浓度为 37 +/- 1 nmol/mg 心脏蛋白，缺血心内膜下心肌 ATP 浓度为 19 +/- 2 nmol/mg。心脏再灌注90分钟和72小时后，再灌注心内膜下ATP仍然显着降低，分别为25+/-5和29+/-2nmol/mg（与ATP保持正常的非缺血区相比，P小于0.05和P小于0.01）。缺血期间 CP 水平下降，但再灌注 90 分钟后恢复正常。缺血期间心肌节段的收缩期缩短百分比从+18 +/- 1%（主动缩短）下降至-13 +/- 2%（被动延长），并且在再灌注72小时时仍显着降低为+11 +/- 1%（与闭塞前相比，P小于0.05）。组织学检查未见坏死，但存在超微结构异常。因此，短暂的心肌缺血与坏死无关，但会导致功能、生化和超微结构异常，这些异常在冠状动脉再灌注后至少持续 3 天。
The purpose of this study was to determine if biochemical, functional, and ultrastructural abnormalities persist in nonnecrotic postischemic myocardium salvaged by coronary reperfusion. Anesthetized dogs were subjected to 15 min of occlusion of the left anterior descending (LAD) coronary artery followed by 3 days of reperfusion. Biopsies were obtained for measurement of adenosine 5'-triphosphate (ATP) and creatine phosphate (CP) nmol/mg protein), and regional function was evaluated using sonomicrometry. Myocardial ATP concentration after 15 min of occlusion was 37 +/- 1 nmol/mg cardiac protein in nonischemic subendocardium and 19 +/- 2 nmol/mg in ischemic subendocardium. After the hearts underwent 90 min and 72 h of reperfusion, ATP remained significantly depressed in reperfused subendocardium with values of 25 +/- 5 and 29 +/- 2 nmol/mg, respectively (P less than 0.05 and P less than 0.01 compared with the nonischemic zone in which ATP remained normal). CP levels fell during ischemia but returned to normal by 90 min of reperfusion. Percent systolic shortening of myocardial segments fell from +18 +/- 1% (active shortening) to -13 +/- 2% (passive lengthening) during ischemia and was still significantly depressed at +11 +/- 1% (P less than 0.05 vs. preocclusion) at 72 h of reperfusion. Histological examination showed no necrosis, but ultrastructural abnormalities were present. Therefore brief periods of myocardial ischemia are not associated with necrosis but result in functional, biochemical, and ultrastructural abnormalities, which are present for at lest 3 days after coronary reperfusion.