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缺血预处理可减小猪心肌梗死面积。

Ischemic preconditioning reduces infarct size in swine myocardium.

作者信息

Schott R J, Rohmann S, Braun E R, Schaper W

机构信息

Max Planck Institute, Department of Experimental Cardiology, Bad Nauheim, FRG.

出版信息

Circ Res. 1990 Apr;66(4):1133-42. doi: 10.1161/01.res.66.4.1133.

Abstract

We evaluated the hypothesis that stunning swine myocardium with brief ischemia reduces oxygen demand in the stunned region and increases tolerance of myocardium to longer periods of ischemia. Wall function was quantified with ultrasonic crystals aligned to measure wall thickening, and stunning was achieved with two cycles of left anterior descending coronary artery (LAD) occlusion (10 minutes) and reperfusion (30 minutes), after which the LAD was occluded for 60 minutes and reperfused for 90 minutes. Infarct size (as a percent of risk region) was then determined by incubating myocardium with para-nitro blue tetrazolium. Regional oxygen demand was measured as myocardial oxygen consumption before the 60-minute LAD occlusion in the stunned region; tracer microspheres were used to determine blood flow, and blood from the anterior interventricular vein and left atrium was used to calculate oxygen saturations. After the second reperfusion period, wall thickening in the stunned region was reduced to 1.4 +/- 2.4% compared with 36.7 +/- 2.5% (mean +/- SEM) before ischemia (p less than 0.001). Regional myocardial oxygen consumption after stunning (3.1 +/- 0.7 ml O2/min/100 g) was no different from regional myocardial oxygen consumption before stunning (3.7 +/- 0.6 ml O2/min/100 g). In the nine pigs "preconditioned" by stunning, infarct size was 10.4 +/- 6.3% of the risk region compared with 48.0 +/- 12.7% in the six control pigs subjected to 60 minutes of ischemia without prior stunning (p less than 0.005). The risk regions were similar (14.4 +/- 1.5% vs. 14.6 +/- 1.9% of the left ventricle, preconditioned vs. control pigs, respectively). We conclude that stunning swine myocardium with two cycles of a 10-minute LAD occlusion followed by reperfusion increases ischemic tolerance but that changes in regional demand in stunned myocardium do not predict the marked reduction in infarct size that follows a subsequent 60-minute period of ischemia.

摘要

我们评估了以下假说

短暂缺血使猪心肌顿抑可降低顿抑区域的氧需求,并增加心肌对更长时间缺血的耐受性。通过排列超声晶体以测量室壁增厚来量化室壁功能,通过左前降支冠状动脉(LAD)闭塞两个周期(10分钟)和再灌注(30分钟)实现心肌顿抑,之后LAD闭塞60分钟并再灌注90分钟。然后通过用对硝基蓝四氮唑孵育心肌来确定梗死面积(占危险区域的百分比)。区域氧需求在顿抑区域LAD闭塞60分钟前作为心肌耗氧量进行测量;用放射性微球测定血流量,并用来自前室间静脉和左心房的血液计算氧饱和度。在第二个再灌注期后,顿抑区域的室壁增厚降至1.4±2.4%,而缺血前为36.7±2.5%(平均值±标准误)(p<0.001)。顿抑后区域心肌耗氧量(3.1±0.7ml O2/min/100g)与顿抑前区域心肌耗氧量(3.7±0.6ml O2/min/100g)无差异。在通过顿抑“预处理”的9头猪中,梗死面积为危险区域的10.4±6.3%,而在6头未经预先顿抑而经历60分钟缺血的对照猪中为48.0±12.7%(p<0.005)。危险区域相似(分别为左心室的14.4±1.5%和14.6±1.9%,预处理猪与对照猪)。我们得出结论,LAD闭塞10分钟后再灌注两个周期使猪心肌顿抑可增加缺血耐受性,但顿抑心肌区域需求的变化并不能预测随后60分钟缺血后梗死面积的显著减少。

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