MICROVASCULAR DETERIORATION - IMPLICATIONS FOR REPERFUSION
MICROVASCULAR DETERIORATION - IMPLICATIONS FOR REPERFUSION
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DOI：
10.1093/cvr/18.5.310
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发表时间：
1984-01-01
影响因子：
10.8
通讯作者：
ROBERTS, R
中科院分区：
文献类型：
--
作者：
FUKUYAMA, T;SOBEL, BE;ROBERTS, R
再灌注或血运重建对急性心肌损伤的有益作用可能仅限于最初的几个小时，部分原因是心肌出血和无复流的发生。使用 51Cr-红细胞评估局部心肌出血的严重程度，并与使用 51 只狗的标记微球评估的相同区域的局部血流进行比较，以确定再灌注引起的出血和无复流与先前缺血持续时间的时间关系。 31只狗在冠状动脉闭塞选定的时间间隔（1-7小时）后开始再灌注，与14只狗的结果相比，结果是持续闭塞，6只狗没有闭塞。用丽丝胺染料粗略地勾勒出灌注减少的区域。连续监测心率、血压和左心房压。通过组织学证实出血。心脏正常区域的血液量为3.2±。湿重的0.4%。在组织缺血1小时而没有再灌注的情况下，它更小，即2.3±。 0.7;闭塞7小时后，这一比例进一步降低至1.3%。在选定的缺血时间间隔后进行再灌注的狗中，缺血3小时后心内膜发生出血（6.6.+-.3.38ml.cntdot.100g-1），但仅在缺血5小时后心外膜发生出血（3.9.+-.1）。缺血 1 小时后再灌注，心内膜区域血流正常 (0.9 .+-. 0.2 ml .cntdot. min-1 .cntdot. g-1)，但再灌注前 7 小时缺血时血流减少 50%。因此，出血发生早于无复流。结果表明，微血管损伤的严重程度是再灌注前缺血间隔持续时间的函数，并且最早在内膜下明显明显。由于出血先于无复流，血液外渗可能导致无复流现象。旨在延缓微血管恶化的辅助措施可能有助于延长有效实施松解术或搭桥手术的时间间隔。
Beneficial effects of reperfusion or revascularization on acute myocardial injury may be restricted to the initial few hours due in part to the development of myocardial hemorrhage and no-reflow. The severity of regional myocardial hemorrhage was assessed with 51Cr-red blood cells and compared with regional flow in the same areas assessed with labeled microspheres in 51 dogs to determine the temporal profile of reperfusion induced hemorrhage and no-reflow in relation to the duration of preceding ischemia. Reperfusion was initiated after selected intervals of coronary occlusion (1-7 h) in 31 dogs, and results compared to those in 14 dogs were persistent occlusion and 6 dogs with no occlusion. Regions of decreased perfusion were outlined grossly with lissamine dye. Heart rate, blood pressure and left atrial pressures were monitored continuously. Hemorrhage was confirmed by histology. The amount of blood in normal regions of the heart was 3.2 .+-. 0.4% of wet weight. In tissue ischemic for 1 h without reperfusion, it was less, i.e., 2.3 .+-. 0.7; with occlusion of 7 h, it was reduced even further to 1.3%. In dogs subjected to reperfusion after selected intervals of ischemia, hemorrhage (6.6 .+-. 3.38 ml .cntdot. 100 g-1) occurred in the endocardium after 3 h of ischemia but in the epicardium only after 5 h of ischemia (3.9 .+-. 1). Regional flow was normal in the endocardium with reperfusion after 1 h of ischemia (0.9 .+-. 0.2 ml .cntdot. min-1 .cntdot. g-1) but decreased by 50% with ischemia of 7 h prior to reperfusion. Thus, hemorrhage occurred earlier than no-reflow. Results indicate that the severity of microvascular damage is a function of the duration of the interval of ischemia prior to reperfusion and that it is evident earliest in the subendocardium. Since hemorrhage preceded no-reflow, extravasation of blood may contribute to the no-reflow phenomenon. Adjunctive measures designed to delay microvascular deterioration may be useful to prolong the interval in which lysis or bypass surgery can be implemented effectively.