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1 Departments of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin, USA
2 Departments of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
3 Departments of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Medicine (Division of Cardiovascular Diseases), Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
4 Departments of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
* To whom correspondence should be addressed. E-mail: jkersten{at}mcw.edu.
We tested the hypothesis that glucose-insulin-potassium (GIK)-induced protection against myocardial infarction depends on ATP-dependent potassium (KATP) channel activation and is abolished by hyperglycemia before the ischemia. Dogs were subjected to a 60 min coronary artery occlusion (CAO) and 3 h reperfusion in the absence or presence of GIK (25% dextrose; 50 IU insulin/L; 80 mM/L KCl infused at 1.5 ml/kg/h) beginning 75 min before CAO or 5 min before reperfusion. The role of KATP channels was evaluated by pretreatment with glyburide (0.1 mg/kg). The efficacy of GIK was investigated with increases in blood glucose concentrations (BG) to 300 or 600 mg/dL or experimental diabetes (alloxan/streptozotocin). Infarct size (IS) was 29±2% of the area at risk (AAR) in control experiments. GIK decreased (P<0.05) IS when administered beginning 5 min before reperfusion. This protective action was independent of BG (13±2 and 12±2% of AAR; BG = 80 or 600 mg/dL, respectively), but was abolished in dogs receiving glyburide (30±4%), hyperglycemia before ischemia (27±4%), or diabetes (25±3%). IS was unchanged by GIK when administered before ischemia independent of BG (31±3, 27±2, and 35±3%; BG = 80, 300, and 600 mg/dL, respectively). The insulin component of GIK promotes cardioprotection by KATP channel activation. However, glucose decreases KATP channel activity, and this effect predominates when hyperglycemia is present before ischemia.
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