LIMITATION OF INFARCT EXPANSION AND VENTRICULAR REMODELING BY LATE REPERFUSION - STUDY OF TIME-COURSE AND MECHANISM IN A RAT MODEL
LIMITATION OF INFARCT EXPANSION AND VENTRICULAR REMODELING BY LATE REPERFUSION - STUDY OF TIME-COURSE AND MECHANISM IN A RAT MODEL
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DOI：
10.1161/01.cir.88.6.2872
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发表时间：
1993-12-01
期刊：
影响因子：
37.8
通讯作者：
WEISMAN, HF
中科院分区：
文献类型：
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作者：
BOYLE, MP;WEISMAN, HF
背景急性梗死心肌的再灌注可能是有益的限制梗死扩大和心室重构，即使建立后的时间，挽救缺血心肌是可能的。为了研究晚期再灌注的持久性、时间过程和机制，将200只大鼠随机分为四组：（1）梗死后1 - 2小时再灌注组，（2）梗死后6 - 8小时再灌注组，（3）梗死后无再灌注组，和（4）假手术组。存活的大鼠在梗死扩展达到平台期的第7天或梗死愈合完成的第21天处死。在7天和21天的分析中，晚期再灌注并没有减少梗死面积或透壁性坏死的程度，但显著限制了梗死扩展，这是通过基于梗死内膜段延长和梗死壁变薄的指数来测量的（7天的扩展指数：无再灌注，2.73+/-0.25，n =13;再灌注1 ~ 2小时后，1.56 ± 0.13，n=23，P
Background. Reperfusion of acutely infarcted myocardium may be beneficial in limiting infarct expansion and ventricular remodeling even if established after the time that salvage of ischemic myocardium is possible.Methods and Results. To examine the permanency, time course, and mechanism of this effect of late reperfusion, 200 rats were randomized into one of four groups: (1) infarction with reperfusion after 1 to 2 hours, (2) infarction with reperfusion after 6 to 8 hours, (3) infarction without reperfusion, and (4) sham operation. Surviving rats were killed at either 7 days, when infarct expansion has plateaued, or 21 days, when infarct healing is complete. In both 7- and 21-day analyses, late reperfusion did not reduce infarct size or degree of transmural necrosis but significantly limited infarct expansion, as measured by an index based on infarct endocardial segment lengthening and infarct wall thinning (expansion index at 7 days: no reperfusion, 2.73+/-0.25, n=13; reperfusion after 1 to 2 hours, 1.56+/-0.13, n=23, P