Alhaddad I A, Tkaczevski L, Siddiqui F, Mir R, Brown E J
Department of Medicine, State University of New York at Stony Brook, Nassau County Medical Center, East Meadow, USA.
Circulation. 1995 Jun 1;91(11):2819-23. doi: 10.1161/01.cir.91.11.2819.
The time window of the benefits of late reperfusion on infarct shape is limited. In rats, these benefits diminish in a wave front over time, with minimal benefits when reperfusion follows 16 hours of coronary occlusion. The mechanism of the benefits of aspirin on survival after acute myocardial infarction is unknown. The purpose of this study was to test the ability of aspirin to enhance the benefits of late coronary artery reperfusion on infarct shape and to examine the mechanism of the benefits of aspirin on infarct shape.
Rats were entered into two different protocols, the morphometric and the histological protocols. In the morphometric protocol, rats were randomized into two groups: the aspirin group, in which rats underwent left coronary artery occlusion followed by treatment with aspirin (12 mg/kg i.v.), and the control group, in which rats underwent left coronary artery occlusion followed by treatment with placebo. Rats in both groups were reperfused 8 hours after coronary occlusion. Rats in the aspirin group received aspirin in the drinking water (12 +/- 2 mg/kg daily). Morphometric analysis was performed 2 weeks after acute myocardial infarction. In the histological protocol, rats underwent the same randomization, coronary occlusion, and reperfusion protocols. Hearts were removed 24 hours after coronary occlusion, and microvessels were assessed for patency. Infarct size expressed as a percent of circumference was similar in the aspirin and placebo treatment groups (28 +/- 2% versus 33 +/- 3%, P = NS). Septal thickness was also similar in both groups (1.8 +/- 0.1 versus 2.1 +/- 0.1 mm, P = NS for aspirin versus placebo). The aspirin-treated group had thicker infarcts compared with the placebo-treated group (0.8 +/- 0.1 versus 0.5 +/- 0.1 mm, P < .05) and less expanded infarcts (expansion index, 1.2 +/- 0.1 versus 2.0 +/- 0.2, P < .05). Aspirin was associated with increased patency of the microvessels in the infarcted area compared with the placebo group (96% versus 64% of microvessels patent, P < .001).
Aspirin enhances the benefit of late coronary artery reperfusion on infarct shape after 8 hours of coronary occlusion. The benefits of aspirin on infarct shape after late reperfusion are related to increased patency of the microvessels in the infarcted area.
晚期再灌注对梗死灶形态的益处的时间窗是有限的。在大鼠中,这些益处会随着时间呈波前状减弱,冠状动脉闭塞16小时后再灌注时益处最小。阿司匹林对急性心肌梗死后生存率的益处机制尚不清楚。本研究的目的是测试阿司匹林增强晚期冠状动脉再灌注对梗死灶形态的益处的能力,并研究阿司匹林对梗死灶形态有益的机制。
将大鼠分为两种不同的方案,即形态学方案和组织学方案。在形态学方案中,大鼠被随机分为两组:阿司匹林组,大鼠先进行左冠状动脉闭塞,然后用阿司匹林(12mg/kg静脉注射)治疗;对照组,大鼠先进行左冠状动脉闭塞,然后用安慰剂治疗。两组大鼠在冠状动脉闭塞8小时后进行再灌注。阿司匹林组的大鼠在饮用水中给予阿司匹林(每日12±2mg/kg)。急性心肌梗死后2周进行形态学分析。在组织学方案中,大鼠进行相同的随机分组、冠状动脉闭塞和再灌注方案。冠状动脉闭塞24小时后取出心脏,评估微血管的通畅情况。阿司匹林治疗组和安慰剂治疗组以周长百分比表示的梗死面积相似(28±2%对33±3%,P=无显著性差异)。两组的室间隔厚度也相似(1.8±0.1对2.1±0.1mm,阿司匹林组与安慰剂组相比P=无显著性差异)。与安慰剂治疗组相比,阿司匹林治疗组的梗死灶更厚(0.8±0.1对0.5±0.1mm,P<0.05),梗死灶扩展更小(扩展指数,1.2±0.1对2.0±0.2,P<0.05)。与安慰剂组相比,阿司匹林与梗死区域微血管通畅性增加有关(微血管通畅率96%对64%,P<0.001)。
冠状动脉闭塞8小时后,阿司匹林可增强晚期冠状动脉再灌注对梗死灶形态的益处。晚期再灌注后阿司匹林对梗死灶形态的益处与梗死区域微血管通畅性增加有关。