Connelly C M, Ngoy S, Schoen F J, Apstein C S
Cardiac Muscle Research Laboratory, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118.
Circ Res. 1992 Aug;71(2):401-13. doi: 10.1161/01.res.71.2.401.
Left ventricular (LV) rupture potential was studied after transmural myocardial infarction (MI) in rabbits by measuring 1) the tensile strength of infarcted tissue strips, 2) the force required to initiate a tear (tear threshold) in the central infarcted region, and 3) the intracavitary pressure required to rupture the infarcted ventricle. During the first week after MI, infarcts resulting from a permanent coronary occlusion were compared with infarcts reperfused "late" (i.e., 3 hours) after coronary occlusion with a resultant hemorrhagic transmural infarct but no reduction in infarct size. The reperfused hemorrhagic infarcted strips had less tensile strength than strips from permanently occluded infarcts in the initial 24 hours after MI (16 +/- 1 versus 24 +/- 3 g/mm2, p less than 0.05), but the tear threshold and response to increased LV pressure were not influenced by infarct reperfusion at this time. By 3 days after MI, reperfused infarcts had equal tensile strength, had greater resistance to infarct tearing, and could withstand a greater LV distending pressure compared with permanently occluded infarcts. By 5 days after MI, reperfused infarcts maintained a greater tear threshold but had less tensile strength than permanently occluded infarcts, although all infarct values were equivalent or greater than normal LV values. By 7 days after MI, reperfused and permanently occluded infarcts were equally strong by all measurements. Thus, late reperfusion of transmural infarcts increased resistance to infarct tearing and LV rupture above that of nonreperfused permanently occluded infarcts by 3 days after MI and enhanced tissue strength after an initial 24-hour vulnerable period. These findings suggest that late reperfusion may accelerate myocardial healing after MI.
通过测量以下指标,研究了兔透壁性心肌梗死(MI)后左心室(LV)破裂的可能性:1)梗死组织条带的抗张强度;2)在梗死中心区域引发撕裂所需的力(撕裂阈值);3)梗死心室破裂所需的腔内压力。在MI后的第一周,将永久性冠状动脉闭塞导致的梗死与冠状动脉闭塞“晚期”(即3小时)再灌注后的梗死进行比较,后者导致出血性透壁梗死,但梗死面积未减小。再灌注出血性梗死条带在MI后的最初24小时内抗张强度低于永久性闭塞梗死的条带(16±1对24±3g/mm2,p<0.05),但此时撕裂阈值和对左心室压力升高的反应不受梗死再灌注的影响。MI后3天,与永久性闭塞梗死相比,再灌注梗死具有相同的抗张强度,对梗死撕裂具有更大的抵抗力,并且能够承受更大的左心室扩张压力。MI后5天,再灌注梗死保持较高的撕裂阈值,但抗张强度低于永久性闭塞梗死,尽管所有梗死值均等于或大于正常左心室值。MI后7天,通过所有测量,再灌注和永久性闭塞梗死的强度相同。因此,透壁性梗死的晚期再灌注在MI后3天增加了对梗死撕裂和左心室破裂的抵抗力,高于未再灌注的永久性闭塞梗死,并在最初24小时的脆弱期后增强了组织强度。这些发现表明,晚期再灌注可能会加速MI后的心肌愈合。