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糖尿病兔心肌对缺血耐受性的改善

Improved myocardial tolerance to ischaemia in the diabetic rabbit.

作者信息

Hadour G, Ferrera R, Sebbag L, Forrat R, Delaye J, de Lorgeril M

机构信息

INSERM U121, Lyon, France.

出版信息

J Mol Cell Cardiol. 1998 Sep;30(9):1869-75. doi: 10.1006/jmcc.1998.0751.

DOI:10.1006/jmcc.1998.0751
PMID:9769241
Abstract

Because cardiac complications after myocardial infarction are more frequent in diabetics, we tested whether experimentally-induced diabetes may increase ischaemic myocardial injury in 23 rabbits. Diabetes was induced in randomized rabbits with the alloxan method. After 2 months, diabetic rabbits underwent a 30-min coronary occlusion followed by 3-h reperfusion and were compared with controls. Collateral flow was measured by the radioactive microsphere technique and infarct size by tetrazolium staining. Infarct size represented 28.6+/-4% of area-at-risk in controls and 16.5+/-3% in diabetics (P<0.05). Collateral flow (0.06+/-0.03 ml/min/g in controls and 0.014+/-0.004 ml/min/g in diabetics) and area-at-risk (50.2+/-4.2% of left ventricle in controls and 53.9+/-5. 4% in diabetics) were similar in both groups. There was a significant positive correlation between area-at-risk and infarct size in both groups (r=0.60 and 0.70, respectively) and for a given area-at-risk, diabetic rabbits developed smaller myocardial infarction than controls (covariance analysis, P<0.01). In additional experiments, hyperglycemia induced by intravenous glucose infusion in non-diabetic rabbits did not protect the ischaemic myocardium (infarct size: 37.9+/-12.5%). In conclusion, diabetes in the rabbit induces a chronic and metabolic form of preconditioning. Further studies are needed to explore the mechanism and time course of this protection.

摘要

由于糖尿病患者心肌梗死后心脏并发症更为常见,我们在23只兔子身上测试了实验性诱导糖尿病是否会增加缺血性心肌损伤。采用四氧嘧啶法对随机分组的兔子诱导糖尿病。2个月后,对糖尿病兔子进行30分钟的冠状动脉闭塞,随后再灌注3小时,并与对照组进行比较。用放射性微球技术测量侧支血流,用四氮唑染色法测量梗死面积。梗死面积在对照组中占危险区域面积的28.6±4%,在糖尿病组中占16.5±3%(P<0.05)。两组的侧支血流(对照组为0.06±0.03 ml/min/g,糖尿病组为0.014±0.004 ml/min/g)和危险区域(对照组占左心室的50.2±4.2%,糖尿病组占53.9±5.4%)相似。两组中危险区域与梗死面积之间均存在显著正相关(分别为r=0.60和0.70),对于给定的危险区域,糖尿病兔子发生的心肌梗死比对照组小(协方差分析,P<0.01)。在额外的实验中,非糖尿病兔子静脉输注葡萄糖诱导的高血糖并未保护缺血心肌(梗死面积:37.9±12.5%)。总之,兔子中的糖尿病诱导了一种慢性代谢形式的预处理。需要进一步研究来探索这种保护的机制和时间进程。

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