Why the study?
Does glucose-insulin-potassium (GIK) infusion improve metabolic and electrocardiographic parameters in a canine model of segmental myocardial ischemia?
Does glucose-insulin-potassium (GIK) infusion improve metabolic and electrocardiographic parameters in a canine model of segmental myocardial ischemia?
In a canine model of partial coronary occlusion, GIK infusion shifts myocardial substrate utilization from free fatty acids to glucose, potentially improving the relationship between myocardial oxygen demand and supply.
GIK metabolic effects in canine ischemia are hypothesis-generating; human trials required before any clinical consideration.
This investigation was designed to explore the metabolic, hemodynamic, and electrocardiographic effects of glucose-insulin-potassium (GIK) solution in a model of segmental myocardial ischemia with significant but incomplete restriction of coronary blood flow. An open-chest anesthetized canine model was utilized including 11 GIK and 6 saline control experiments. The anterior descending coronary artery (LAD) was partially occluded causing an average 71% reduction in its blood flow. Thirty min following occlusion GIK or saline was infused for 30 min at 3 ml/min into a femoral vein. Statistically significant effects of GIK included: increased glucose uptake by the ischemic myocardium, reduced arterial free fatty acid (FFA) concentration, reduced myocardial FFA uptake, decreased coronary arterio-venous oxygen content difference, increased myocardial lactate extraction, decreased myocardial potassium egress, and reduced epicardial ST segment elevation. Heart rate, aortic and left ventricular end-diastolic pressures, and developed force in the ischemic area were unchanged. The results indicate a potentially favorable effect of GIK on the metabolism of the ischemic myocardium which may be due to the shift of substrate utilization from free fatty acids to glucose.
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Haneda et al. (1978) studied this question.
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