Richard V, Murry C E, Reimer K A
Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA.
Circulation. 1995 Oct 1;92(7):1891-901. doi: 10.1161/01.cir.92.7.1891.
Early reperfusion salvages ischemic myocardium and limits myocardial infarct size. However, the effects of late reperfusion, after the possibility for limitation of infarct size has passed, have not been completely elucidated. The purpose of this study was to ascertain the effect of reperfusion after 6 hours of ischemia on the rate of infarct healing and on the size and geometry of the resulting scars, as determined by gross and microscopic quantification.
Myocardial infarcts were produced in anesthetized, open-chest dogs by occlusion of the circumflex coronary artery. They either were reperfused by removal of the occluding snare or were nonreperfused. The animals were allowed to recover for either 4 days, 2 weeks, or 6 weeks. At these times, infarct size, infarct dimensions (wall thickness and circumferential extent), and the proportion of infarct occupied by necrotic myocardium versus granulation tissue (evolving scar) were measured. At 4 days, infarcts were swollen in both nonreperfused and reperfused groups (increased thickness and circumferential extent of the area at risk). Conversely, at 6 weeks, the size, thickness, and circumferential extent of the scar all were decreased. Two common anatomic complications of human infarction, cardiac rupture and chronic infarct expansion (aneurysm), did not occur in this experimental model. Reperfusion at 6 hours did not affect initial infarct size (4 days) or scar size (6 weeks). At 2 weeks, reperfused infarcts were smaller and were composed of proportionately more granulation tissue and less nonresorbed necrosis than nonreperfused infarcts.
Thus, reperfusion accelerated the rate of infarct repair, ie, the replacement of necrotic myocardium by scar. Acceleration of infarct repair may be a beneficial effect of late reperfusion even after the opportunity for limitation of infarct size has passed.
早期再灌注可挽救缺血心肌并限制心肌梗死面积。然而,在限制梗死面积的可能性已经过去之后的晚期再灌注的影响尚未完全阐明。本研究的目的是通过大体和显微镜定量确定缺血6小时后再灌注对梗死愈合速率以及所形成瘢痕的大小和几何形状的影响。
通过结扎左旋冠状动脉在麻醉开胸犬中产生心肌梗死。它们要么通过移除结扎圈套进行再灌注,要么不进行再灌注。让动物恢复4天、2周或6周。在这些时间点,测量梗死面积、梗死尺寸(壁厚和圆周范围)以及坏死心肌与肉芽组织(正在形成的瘢痕)所占梗死面积的比例。在4天时,未再灌注组和再灌注组的梗死均肿胀(危险区域的厚度和圆周范围增加)。相反,在6周时,瘢痕的大小、厚度和圆周范围均减小。人类梗死的两种常见解剖学并发症,心脏破裂和慢性梗死扩展(动脉瘤),在该实验模型中未发生。6小时时的再灌注不影响初始梗死面积(4天)或瘢痕面积(6周)。在2周时,再灌注的梗死较小,与未再灌注的梗死相比,其肉芽组织比例更高,未吸收的坏死组织更少。
因此,再灌注加速了梗死修复速率,即坏死心肌被瘢痕替代。即使在限制梗死面积的机会已经过去之后,加速梗死修复可能是晚期再灌注的有益效果。