Recovery from prolonged abnormalities of canine myocardium salvaged from ischemic necrosis by coronary reperfusion.
Recovery from prolonged abnormalities of canine myocardium salvaged from ischemic necrosis by coronary reperfusion.
复制标题
通过冠状动脉再灌注从缺血性坏死中挽救的犬心肌的长期异常中恢复。
DOI：
--
复制
发表时间：
1981
影响因子：
11.1
通讯作者：
E. Braunwald
中科院分区：
文献类型：
--
作者：
R. Kloner;L. Deboer;J. R. Darsee;J. Ingwall;E. Braunwald
本研究的目的是确定短暂暂时性冠状动脉闭塞（与坏死无关）所产生的生化、功能和超微结构异常是否会消退，如果会，则何时消退。麻醉开胸犬进行15分钟冠状动脉闭塞，然后进行72小时、7天或14天的再灌注。连续进行活体心肌活检以测量ATP并进行超微结构分析。用声速测量法评价区域功能。缺血15 min后，非缺血性心内膜下心肌ATP平均（+/- SEM）浓度为36.6 +/- 1.2 nmol/mg，缺血性心内膜下为18.9 +/- 1.5 nmol/mg。ATP残留用于ATP测量和超微结构分析。用声速测量法评价区域功能。缺血15 min后，非缺血性心内膜下心肌ATP平均（+/- SEM）浓度为36.6 +/- 1.2 nmol/mg，缺血性心内膜下为18.9 +/- 1.5 nmol/mg。ATP残留用于ATP测量和超微结构分析。用声速测量法评价区域功能。缺血15 min后，非缺血性心内膜下心肌ATP平均（+/- SEM）浓度为36.6 +/- 1.2 nmol/mg，缺血性心内膜下为18.9 +/- 1.5 nmol/mg。在缺血前再灌注的心内膜下，ATP在90分钟（非缺血值的68%）和72小时（非缺血值的78%）仍处于抑制状态，但在7天恢复正常。局部收缩功能和心脏超微结构异常需要7天才能完全恢复。组织学及组织化学分析均未见坏死。因此，短暂性冠状动脉闭塞引起的与坏死无关的生化、功能和超微结构异常可以完全消除，但恢复期延长。
The purpose of this study was to determine whether or not the biochemical, functional, and ultrastructural abnormalities produced by brief temporary coronary occlusions (unassociated with necrosis) ever resolve and, if so, when they do. Anesthetized open-chest dogs were subjected to 15 min of coronary artery occlusion followed by 72 hr, 7 days, or 14 days of reperfusion. Serial in vivo myocardial biopsies were performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remainede performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remainede performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (+/- SEM) myocardial ATP concentration was 36.6 +/- 1.2 nmol/mg of cardiac protein in nonischemic subendocardium and 18.9 +/- 1.5 in ischemic subendocardium after 15 min of ischemia. ATP remained depressed in the reperfused previously ischemic subendocardium at both 90 min (68% of nonischemic value) and 72 hr (78% of nonischemic value) but returned to normal at 7 days. Regional systolic function and cardiac ultrastructural abnormalities required 7 days for full recovery. Histologic and histochemical analysis did not reveal necrosis at any time. Therefore, biochemical, functional, and ultrastructural abnormalities induced by brief periods of transient coronary occlusion not associated with necrosis do resolve completely but the recovery period is prolonged.