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在动脉再灌注前进行缺氧再灌注以清除缺血性分解代谢产物,并不会限制犬类心肌梗死的面积。

Hypoxic reperfusion to remove ischaemic catabolites prior to arterial reperfusion does not limit the size of myocardial infarcts in dogs.

作者信息

Tanaka M, Earnhardt R C, Murry C E, Richard V J, Jennings R B, Reimer K A

机构信息

Department of Pathology, Duke University Medical Center, Durham, NC 27710.

出版信息

Cardiovasc Res. 1991 Jan;25(1):7-16. doi: 10.1093/cvr/25.1.7.

Abstract

STUDY OBJECTIVE

Although timely reperfusion limits myocardial infarct size, it has been postulated that reperfusion itself may kill some myocytes which were alive at the end of an episode of ischaemia (lethal reperfusion injury). The aim of this study was to test the hypothesis that ischaemic catabolites may "prime" myocardium for such injury and that preliminary hypoxic washout of such catabolites, prior to arterial reperfusion, would limit myocardial infarct size.

DESIGN

Dogs underwent a 40 min occlusion of the left circumflex coronary artery, followed by 4 d reperfusion. In a treated group, a 5 min episode of coronary artery perfusion with hypoxic buffer was instituted at the end of this ischaemic episode, before blood reperfusion was restored. Control dogs received a similar volume of hypoxic buffer intravenously. Systemic fluid overload was attenuated by haemofiltration. The effect of this preliminary hypoxic washout on myocardial infarct size was assessed.

EXPERIMENTAL MATERIAL

18 anaesthetised, open chest dogs were used. After the acute study they recovered from surgery for 4 d and were then killed for further study.

MEASUREMENTS AND MAIN RESULTS

Infarct size, determined by microscopic evaluation, was not significantly different in the two groups, at (control) 31.3 (SEM 6.2)% v (hypoxic reperfusion) 25.8(3.9)% of the vascular area at risk. In control dogs, infarct size was inversely related to the amount of collateral blood flow (measured using microspheres); hypoxic reperfusion did not shift this relation (analysis of covariance, F = 0.236, NS).

CONCLUSIONS

The washout of ischaemic catabolites by hypoxic perfusate prior to reoxygenation did not limit infarct size.

摘要

研究目的

尽管及时再灌注可限制心肌梗死面积,但据推测,再灌注本身可能会杀死一些在缺血期结束时仍存活的心肌细胞(致死性再灌注损伤)。本研究的目的是检验以下假设:缺血代谢产物可能使心肌对这种损伤产生“预适应”,并且在动脉再灌注之前对这些代谢产物进行初步的低氧清除可限制心肌梗死面积。

设计

对犬进行左旋冠状动脉40分钟的闭塞,随后进行4天的再灌注。在一个治疗组中,在恢复血液再灌注之前,在缺血期结束时用低氧缓冲液进行5分钟的冠状动脉灌注。对照犬静脉注射等量的低氧缓冲液。通过血液滤过减轻全身性液体过载。评估这种初步低氧清除对心肌梗死面积的影响。

实验材料

使用18只麻醉的、开胸犬。急性研究后,它们从手术中恢复4天,然后处死以进行进一步研究。

测量和主要结果

通过显微镜评估确定的梗死面积,两组无显著差异,对照组为危险血管区域的31.3(标准误6.2)%,低氧再灌注组为25.8(3.9)%。在对照犬中,梗死面积与侧支血流量(使用微球测量)呈负相关;低氧再灌注并未改变这种关系(协方差分析,F = 0.236,无显著性差异)。

结论

在复氧前用低氧灌注液清除缺血代谢产物并未限制梗死面积。

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