MYOCARDIAL INFARCT EXTENSION DURING REPERFUSION AFTER CORONARY-ARTERY OCCLUSION - PATHOLOGICAL EVIDENCE
MYOCARDIAL INFARCT EXTENSION DURING REPERFUSION AFTER CORONARY-ARTERY OCCLUSION - PATHOLOGICAL EVIDENCE
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DOI：
10.1016/0735-1097(93)90253-w
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发表时间：
1993-04-01
影响因子：
24
通讯作者：
VIRMANI, R
中科院分区：
文献类型：
--
作者：
FARB, A;KOLODGIE, FD;VIRMANI, R
目标。本研究的目的是证明同一动物再灌注期间心肌梗塞的扩展。背景。心肌再灌注是否会导致心肌坏死范围扩大仍存在争议。再灌注后可逆性损伤的心肌细胞向不可逆性损伤的细胞的转化一直难以通过病理学证明。方法。新西兰白兔（第一组，n = 10）接受 30 分钟的冠状动脉闭塞和 180 分钟的再灌注。辣根过氧化物酶是一种渗透到不可逆损伤的心肌细胞肌膜中的示踪蛋白，用于在再灌注开始时定量心肌细胞坏死。在同一心脏内，再灌注 180 分钟后，通过氯化三苯基四唑 (TTC) 染色测量梗塞面积。在单独的实验中，为了证明模型的有效性，对家兔进行30分钟的冠状动脉闭塞，然后静脉输注辣根过氧化物酶并快速诱导死亡（组II）或闭塞30分钟，再灌注180分钟，再灌注180分钟后给予辣根过氧化物酶再灌注，诱导死亡后进行TTC染色（组III）。结果。在第一组中，再灌注开始时由辣根过氧化物酶描绘的梗塞面积测量为风险区域的 45.3 +/- 2.8%，并且显着小于再灌注 180 分钟后 TTC 描绘的梗塞面积（59.8 +/- 3.3%，p = 0.0002）。通过电子显微镜观察，缺血床内的边界区域显示出不可逆损伤的辣根过氧化物酶阳性肌细胞与不可逆损伤的辣根过氧化物酶阴性肌细胞相邻，这表明在再灌注过程中发生了进一步的细胞死亡。在第II组中，冠状动脉闭塞30分钟后由辣根过氧化物酶描绘的梗塞的大小与第I组中用该示踪剂测量的梗塞的大小相似。在第III组中，在再灌注180分钟时由辣根过氧化物酶描绘的梗塞的大小与由TTC测量的梗塞的大小相似，并且与在再灌注180分钟时由TTC描绘的梗塞的大小相似。 I 组再灌注。结论。这些结果提供的证据表明，缺血区域内的边界区域中有一部分肌细胞在再灌注开始时是可行的，但随后在再灌注期间发展为不可逆损伤。
Objectives. The goal of this study was to demonstrate myocardial infarct extension during reperfusion within the same animal.Background. Whether myocardial reperfusion can result in the extension of myocardial necrosis remains controversial. The transformation of reversibly injured myocytes into irreversibly damaged cells after reperfusion has been difficult to demonstrate pathologically.Methods. New Zealand White rabbits (Group I, n = 10) were subjected to 30 min of coronary artery occlusion and 180 min of reperfusion. Horseradish peroxidase, a tracer protein that permeates the sarcolemma of irreversibly injured myocytes, was used to quantitate myocyte necrosis at the beginning of reperfusion. Within the same heart, infarct size was measured after 180 min of reperfusion by triphenyltetrazolium chloride (TTC) staining. In separate experiments to demonstrate the validity of the model, rabbits were subjected to 30 min of coronary occlusion, followed by intravenous infusion of horseradish peroxidase and rapid induction of death (Group II) or 30 min of occlusion, 180 min of reperfusion with horseradish peroxidase administered after 180 min of reperfusion and TTC staining after induced death (Group III).Results. In Group I, infarct size at the onset of reperfusion, delineated by horseradish peroxidase, measured 45.3 +/- 2.8% of the area of risk and was significantly less than TTC-delineated infarct size after 180 min of reperfusion (59.8 +/- 3.3%, p = 0.0002). By electron microscopy, border areas within the ischemic bed demonstrated irreversibly injured horseradish peroxidase-positive myocytes adjacent to irreversibly injured horseradish peroxidase-negative myocytes, suggesting that further cell death occurred during reperfusion. In Group II, infarcts delineated by horseradish peroxidase after 30 min of coronary occlusion were similar in size to infarcts measured by this tracer in Group I. In Group III, infarcts delineated by horseradish peroxidase at 180 min of reperfusion were similar in size to infarcts measured by TTC and similar to TTC-delineated infarcts measured at 180 min of reperfusion in Group I.Conclusions. These results provide evidence that there is a subset of myocytes in border areas within the ischemic region that are viable at the beginning of reperfusion but subsequently progress to irreversible injury during the reperfusion period.