de Lorgeril M, Rousseau G, Basmadjian A, St-Jean G, Tran D C, Latour J G
Laboratory of Experimental Pathology, Montreal Heart Institute, Quebec, Canada.
Am J Cardiovasc Pathol. 1990;3(2):143-54.
To elucidate further the pathogenic role of neutrophils in evolving reperfused myocardial infarction, we investigated the dynamics of their accumulation and distribution in the ischemic myocardium. The left anterior descending coronary artery was occluded in dogs for 2 hours followed by reperfusion for 0, 3, 6, or 24 hours. 111In-labeled neutrophils were injected at the time of occlusion or after 16 hours of reperfusion. The area at risk was similar among groups. Infarct size expressed in percent of the area at risk was identical between groups reperfused for 6 (35.2 +/- 4.4%) or 24 (32.3 +/- 3.9%) hours but smaller (22.0 +/- 4.4%; p less than 0.05) after 3 hours of reperfusion. 111In-neutrophils accumulation quantified by scintigraphy correlated positively with infarct size (r = 0.64, p less than 0.005); accumulation rates (cells/h/cm2MI) were high during the first 3 (2288 +/- 754) and 6 hours (1953 +/- 463) but low (490 +/- 192) between 16 and 24 hours of reperfusion. Cells accumulating during reperfusion (12,566 +/- 2307 cells/g at 3 hours) were found within the borders of the necrotic area, and the cell counts (2420 +/- 724 cells/g, p less than 0.05) in the live tissue located within the area at risk after 3 hours of reperfusion were similar to those found in the subepicardium at the onset of reperfusion: (2240 +/- 571 cells/g). Only a few cells were detected in the normally perfused myocardium (67 +/- 33 cells/g). We conclude that reperfusion accumulation in the ischemic myocardium; the reaction takes place within 3-6 hours of reperfusion, a period of time where infarct size is growing by about 40%. These results support the concept that leukocytes may play a pathogenic role on infarct size in models with brief ischemia followed by reperfusion.
为了进一步阐明中性粒细胞在进展性再灌注心肌梗死中的致病作用，我们研究了它们在缺血心肌中的聚集和分布动态。在犬身上，将左冠状动脉前降支闭塞2小时，然后再灌注0、3、6或24小时。在闭塞时或再灌注16小时后注射铟 - 111标记的中性粒细胞。各实验组之间的危险区域相似。再灌注6小时（35.2±4.4%）或24小时（32.3±3.9%）的实验组中，梗死面积占危险区域的百分比相同，但再灌注3小时后的梗死面积较小（22.0±4.4%；p＜0.05）。通过闪烁扫描定量的铟 - 111中性粒细胞聚集与梗死面积呈正相关（r = 0.64，p＜0.005）；聚集率（细胞数/小时/平方厘米心肌梗死面积）在再灌注的前3小时（2288±754）和6小时（1953±463）较高，但在再灌注16至24小时之间较低（490±192）。再灌注期间聚集的细胞（3小时时为12,566±2307个细胞/克）出现在坏死区域的边界内，再灌注3小时后，危险区域内存活组织中的细胞计数（2420±724个细胞/克，p＜0.05）与再灌注开始时心外膜下的细胞计数相似：（2240±571个细胞/克）。在正常灌注的心肌中仅检测到少数细胞（67±33个细胞/克）。我们得出结论，缺血心肌中存在再灌注聚集现象；这种反应在再灌注的3 - 6小时内发生，在此期间梗死面积大约增加40%。这些结果支持这样的概念，即在短暂缺血后再灌注的模型中，白细胞可能对梗死面积起致病作用。
