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再灌注对缺血心肌的挽救作用:闭塞期间侧支血流和心肌需氧量的重要性。

Salvage of ischaemic myocardium by reperfusion: importance of collateral blood flow and myocardial oxygen demand during occlusion.

作者信息

Przyklenk K, Vivaldi M T, Schoen F J, Malcolm J, Arnold O, Kloner R A

出版信息

Cardiovasc Res. 1986 Jun;20(6):403-14. doi: 10.1093/cvr/20.6.403.

Abstract

Early reperfusion after coronary artery occlusion is used to treat acute myocardial infarction, but the factors that determine whether salvage of ischaemic myocardium actually occurs remain poorly defined. Differences in collateral blood flow to the region at risk, and haemodynamic variables during occlusion, may contribute to uncertainty as to the time beyond which reperfusion no longer reduces infarct size. To clarify this issue, open chest anaesthetised dogs underwent 1, 2, 3, 4, or 6 hours of left anterior descending coronary artery occlusion followed by reperfusion or permanent occlusion (n = 8 per group). Microspheres were injected before occlusion and 15 minutes after occlusion for regional myocardial blood flow determination, and heart rate and arterial blood pressure were measured before occlusion and 10 minutes and 30 minutes after occlusion. At 96 hours after occlusion haemodynamic variables were again measured; the animals were then killed, and occluded bed size was determined by in vitro dye perfusion. The area of necrosis was quantified from histological sections and expressed as a percentage of occluded bed size (AN/OB). If duration of occlusion is considered alone, reperfusion beyond two hours did not salvage ischaemic myocardium in this model. If the results for occlusion equal to and greater than two hours are combined, the mean area of necrosis (27(2)%) was significantly greater than that produced by one hour of occlusion followed by reperfusion (10(4)%). For the animals undergoing occlusion for two or more hours or permanent occlusion, collateral blood flow significantly influenced the area of necrosis. When epicardial flow during occlusion was high (greater than 0.30 ml X min-1 X g-1 tissue) 13 out of 14 dogs undergoing occlusion for two or more hours or permanent occlusion developed small (AN/OB less than 27%) infarcts (mean AN/OB 17(2)%). In contrast, when epicardial collateral flow was low (less than 0.30 ml X min-1 X g-1) 14 out of 23 animals had large (AN/OB greater than 27%) infarcts (mean AN/OB 34(3)%). For the 23 dogs in which epicardial flow was low, heart rate during occlusion significantly influenced infarct size: the 14 dogs that developed large infarcts (AN/OB greater than 27%) had a higher mean heart rate (152(6) beats X min-1) than the nine that developed small infarcts (AN/OB less than 27%) (130(5) beats X min-1; p less than 0.025). Thus reperfusion at one hour after occlusion salvaged ischaemic myocardium.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

冠状动脉闭塞后早期再灌注用于治疗急性心肌梗死,但决定缺血心肌是否真正得到挽救的因素仍不清楚。梗死相关区域侧支血流的差异以及闭塞期间的血流动力学变量,可能导致关于再灌注不再减少梗死面积的时间存在不确定性。为阐明这一问题,对开胸麻醉的犬进行左前降支冠状动脉闭塞1、2、3、4或6小时,随后再灌注或永久闭塞(每组n = 8)。在闭塞前和闭塞后15分钟注射微球以测定局部心肌血流,并在闭塞前、闭塞后10分钟和30分钟测量心率和动脉血压。在闭塞后96小时再次测量血流动力学变量;然后处死动物,通过体外染料灌注确定闭塞心肌床大小。从组织学切片定量坏死面积,并表示为闭塞心肌床大小的百分比(AN/OB)。如果仅考虑闭塞时间,在该模型中,闭塞超过两小时后再灌注并不能挽救缺血心肌。如果将闭塞两小时及以上的结果合并,平均坏死面积(27(2)%)显著大于闭塞一小时后再灌注产生的坏死面积(10(4)%)。对于闭塞两小时及以上或永久闭塞的动物,侧支血流显著影响坏死面积。当闭塞期间的心外膜血流较高(大于0.30 ml·min-1·g-1组织)时,14只接受闭塞两小时及以上或永久闭塞的犬中有13只发生小梗死(AN/OB小于27%)(平均AN/OB 17(2)%)。相反,当心外膜侧支血流较低(小于0.30 ml·min-1·g-1)时,23只动物中有14只发生大梗死(AN/OB大于27%)(平均AN/OB 34(3)%)。对于23只心外膜血流较低的犬,闭塞期间的心率显著影响梗死面积:14只发生大梗死(AN/OB大于27%)的犬的平均心率(152(6)次·min-1)高于9只发生小梗死(AN/OB小于27%)的犬(130(5)次·min-1;p小于0.025)。因此,闭塞后一小时再灌注可挽救缺血心肌。(摘要截断于400字)

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