Higginson L A, White F, Heggtveit H A, Sanders T M, Bloor C M, Covell J W
Circulation. 1982 Jan;65(1):62-9. doi: 10.1161/01.cir.65.1.62.
Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitative reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium. Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.
实验性急性心肌梗死再灌注时常常发生心肌内出血,并且被认为与坏死范围扩大有关。为了确定出血是否与坏死范围扩大相关,20只麻醉犬在冠状动脉回旋支闭塞6小时后进行再灌注,另外10只犬进行对照性闭塞且不进行再灌注。20只再灌注犬中有15只出现肉眼可见的出血,而对照犬均未出现。在12只再灌注犬和10只对照犬中,冠状动脉闭塞后注射放射性微球以定量侧支血流,在再灌注组中注射微球以定量再灌注血流。8只再灌注犬和10只对照犬获得了完整的血流数据。冠状动脉闭塞24小时后,对梗死区和对照区的1克组织段进行出血、侧支血流和肌酸激酶活性分析。另外8只犬在6小时后进行再灌注,随后进行系列显微镜检查,以确定出血是否发生在显微镜下原本正常的心肌中。病理检查表明,出血并未发生在显微镜下原本正常的心肌中。在有出血的犬中,出血程度与心肌肌酸激酶浓度和侧支血流呈负相关。47个出血组织段的平均侧支血流为4.5毫升/100克(为对照的4.2%)。36个出血组织段的平均肌酸激酶为233毫国际单位/克(为对照的21%)。在侧支血流超过对照21%或肌酸激酶超过对照37%的区域未发现出血。出血组织段的平均再灌注血流为对照血流的78.5%。这些研究表明,再灌注时的出血与严重心肌坏死以及再灌注前血流显著降低有关,因此仅发生在再灌注时已明显受损的心肌中。没有证据表明出血发生在再灌注前血流正常甚至轻度降低的区域。