Solares J, Garcia-Dorado D, Oliveras J, González M A, Ruiz-Meana M, Barrabés J A, Gonzalez-Bravo C, Soler-Soler J
Servicio de Cardiología, Hospital General Universitario Vall d'Hebron, Barcelona, Spain.
Virchows Arch. 1995;426(4):393-9. doi: 10.1007/BF00191349.
The aim of this study was to test the hypothesis that increased mechanical stress at the lateral borders of the area at risk may render this area more susceptible to ischaemia/reperfusion injury in the absence of collateral flow. The spatial distribution of myocardial necrosis within the territory of a transiently occluded left anterior descending coronary artery was investigated in 31 porcine hearts submitted to 48 min of coronary occlusion and 6 h of reperfusion. Immediately before excising the heart, the left anterior descending coronary artery was re-occluded and 10% fluorescein was injected in the left atrium. The area at risk was imaged by ultraviolet illumination of the myocardial slices, and the area of necrosis by incubation in triphenyltetrazolium chloride. The area at risk was divided in four sectors and an index of eccentricity was calculated as the percent of the area of necrosis located in the two lateral sectors of the area at risk. The area of contraction band necrosis was measured in whole heart histological sections. Infarcts were generally small, and were composed almost exclusively of contraction band necrosis. There was a good correlation between the extent of the area of contraction band necrosis and infarct size (r = 0.831, P < 0.0005). The area of necrosis had a patchy appearance and was predominantly distributed along the lateral borders of the area at risk. This eccentric distribution was more prominent in smaller infarcts, and the eccentricity index was inversely correlated with infarct size (r = -0.471, P = 0.007), suggesting that contraction band necrosis occurs first at the interface between control and reperfused myocardium in this model. These results are in agreement with a prominent role of mechanical factors in the genesis of myocardial necrosis during transient coronary occlusion.
在没有侧支血流的情况下,危险区域外侧边缘机械应力增加可能使该区域更易发生缺血/再灌注损伤。在31头猪心脏中进行研究,这些心脏经历48分钟冠状动脉闭塞和6小时再灌注,研究左前降支冠状动脉短暂闭塞区域内心肌坏死的空间分布。在切除心脏前即刻,再次闭塞左前降支冠状动脉,并于左心房注射10%荧光素。通过对心肌切片进行紫外线照射成像危险区域,通过在氯化三苯基四氮唑中孵育成像坏死区域。将危险区域分为四个扇形区,并计算偏心率指数,即坏死区域位于危险区域两个外侧扇形区的面积百分比。在全心组织学切片中测量收缩带坏死面积。梗死灶通常较小,几乎完全由收缩带坏死组成。收缩带坏死面积与梗死灶大小之间存在良好相关性(r = 0.831,P < 0.0005)。坏死区域呈斑片状,主要沿危险区域外侧边缘分布。这种偏心分布在较小梗死灶中更明显,且偏心率指数与梗死灶大小呈负相关(r = -0.471,P = 0.007),提示在该模型中收缩带坏死首先发生在对照心肌和再灌注心肌的界面处。这些结果与机械因素在短暂冠状动脉闭塞期间心肌坏死发生过程中起重要作用相一致。