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This Article Full Text Full Text (PDF) All Versions of this Article: 294/5/H2336    most recent 00481.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by du Toit, E. F. Articles by Lochner, A. PubMed PubMed Citation Articles by du Toit, E. F. Articles by Lochner, A.

Myocardial susceptibility to ischemic-reperfusion injury in a prediabetic model of dietary-induced obesity

Departments of ¹Biomedical Sciences, ²Anatomy, and ³Cardiology, Faculty of Health Sciences, University of Stellenbosch, Tygerberg; and ⁴Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa

Submitted 23 April 2007 ; accepted in final form 19 March 2008

We assessed the myocardial susceptibility to ischemic-reperfusion injury in obese rat hearts in the absence and the presence of predicted circulating concentrations of insulin and fatty acids. Feeding rats a high-calorie diet resulted in increases in body weight, visceral fat content, cardiac hypertrophy, plasma insulin, nonesterified free fatty acid, and triglyceride concentrations. In the absence of both insulin and fatty acids in the coronary perfusate, the hearts of obese rats developed an increased infarct size (41.9 ± 1.9% for obese vs. 22.9 ± 2.3% for control, P < 0.05) and a reduced percent recovery of aortic output (4.2 ± 4.2% for obese vs. 27.7 ± 3.4% for controls, P < 0.05) after coronary artery occlusion and reperfusion. In the presence of insulin in the coronary perfusate, a cardioprotective effect was noted in both groups, an action that was greater in hearts from obese compared with control rats and which abolished the obesity-induced changes in infarct size (13.8 ± 1.2% for controls vs. 21.0 ± 1.6% for obese), and percent recovery of aortic output (60.2 ± 4.7% for controls vs. 45.7 ± 9.4% for obese). Fatty acids (0.7 mM, control; and 1.5 mM, obese) added to the coronary perfusate with in vivo concentrations of insulin dramatically increased infarct size (48.2 ± 3.1% for obese, and 37.5 ± 2.7% for control; P < 0.05 vs. without fatty acids) and decreased percent aortic output recovery (control, 10.4 ± 5.2%, and obese 7.8 ± 3.5%; P < 0.05 vs. without fatty acids) in both groups to similar values. In conclusion, in obesity, the impact of an increased susceptibility of the myocardium to ischemic-reperfusion injury on myocardial injury is likely to be overshadowed by the comparatively greater roles played by predicted increases in circulating insulin and fatty acids found in vivo. These data support the notion that adiposity per se is unlikely to be a valuable predictor of outcomes in ischemic-reperfusion injury.

insulin resistance; myocardial infarction; cardiac function