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1 Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
2 Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Physiology and Biophysics, Clinical Nutrition Research Center, The Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: jchatham{at}uab.edu.
The aim of this study was to determine whether the transition from insulin resistance to hyperglycemia in a model of Type-2 diabetes, leads to intrinsic changes in the myocardium that increase the sensitivity to ischemic injury. Hearts from 6, 12 and 24 week old lean (Control) and obese Zucker diabetic fatty (ZDF) rats were isolated, perfused and subjected to 30 min low flow ischemia (LFI) and 60 min reperfusion. At 6 weeks ZDF animals were insulin resistant but not hyperglycemic. By12 weeks the ZDF group was hyperglycemic and became progressively worse by 24 weeks. In spontaneously beating hearts rate-pressure-product (RPP) was depressed in the ZDF groups compared to age matched Controls primarily due to lower heart rate. Pacing significantly increased RPP in all ZDF groups; however, there was also a significant decrease in left ventricular developed pressure to Control. There was also greater contracture during LFI in the ZDF groups compared to the Control; surprisingly however, functional recovery upon reperfusion was significantly higher in the diabetic 12 and 24-week ZDF groups compared to age matched Control groups and the 6-week ZDF group. This improvement in recovery in the ZDF diabetic groups was independent of substrate availability, severity of ischemia and duration of diabetes. These data demonstrate that while the development of Type-2 diabetes lead to progressive contractile and metabolic abnormalities during normoxia and LFI, this was not associated with increased susceptibility to ischemic injury.
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