Why the study?
Do glucose-insulin-potassium (GIK) solutions improve infarct size and ventricular function in isolated hearts with regional ischemia?
Do glucose-insulin-potassium (GIK) solutions improve infarct size and ventricular function in isolated hearts with regional ischemia?
Glucose-insulin-potassium solutions may protect acutely ischemic myocardium by preserving cellular function and improving perfusion during surgical revascularization.
GIK effects in isolated ischemic hearts warrant human trials; should not yet change revascularization practice.
"Surgical myocardial stunning" represents a model of both ischemia and infarction that unlike regular "stunning" has the potential for permanent or partially reversible cellular function. While substrate enhancement may not play an important role in myocardial stunning, it may be critical during surgical stunning when mitochondrial dysfunction is present. The primary myocardial substrate for the normal myocardium is free fatty acids; however, this may not be the optimal energy source for the ischemic heart. Exogenous glucose appears to be a superior substrate during periods of myocardial ischemia. Glucose-insulin-potassium (GIK) solutions appear to have an important role in the revascularization of acutely ischemic myocardium. In isolated hearts with regional ischemia, GIK was shown to decrease infarct size, increase ATP and creatine phosphate levels, and improve ventricular function. GIK appears to protect the ischemic myocardium by preserving cellular function and improving myocardial perfusion. Our preliminary experimental studies indicate that GIK may effectively reduce necrosis and stunning in a model of acute surgical revascularization.
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Harold L. Lazar (1994) studied this question.
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