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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01130.2001
Submitted on December 30, 2001
Accepted on January 21, 2002
1 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Anesthesiology, Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, WI, USA
3 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA; Medicine, Medical College of Wisconsin, Milwaukee, WI, USA
4 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
Volatile anesthetics stimulate but hyperglycemia attenuates the activity of mitochondrial KATP channels. We tested the hypothesis that diabetes mellitus interferes with isoflurane-induced preconditioning. Acutely-instrumented, barbiturate-anesthetized dogs were randomly assigned to receive 0, 0.32, or 0.64% end-tidal concentrations of isoflurane in the absence or presence of diabetes (3 wk after administration of alloxan and streptozotocin) in 6 experimental groups. All dogs were subjected to a 60 min left anterior descending coronary artery occlusion followed by 3 hr of reperfusion. Myocardial infarct size (triphenyltetrazolium staining) was 29±3% (n=8) of the left ventricular area at risk in control experiments. Isoflurane reduced infarct size (15±2 and 13±1% during 0.32 and 0.64% concentrations; n=8 and 7, respectively). Diabetes alone did not alter infarct size (30±3%; n=8) but blocked the protective effects of 0.32% (27±2%; n=7) and not 0.64% isoflurane (18±3%; n=7). Infarct size was directly related to blood glucose concentrations in diabetic dogs, but this relationship was abolished by higher concentrations of isoflurane. The results indicate that blood glucose and end-tidal isoflurane concentrations are important determinants of infarct size during anesthetic-induced preconditioning.
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