Key result
Glucose-KCl-insulin maintains normal sarcosomal oxygen consumption and oxidative phosphorylation in canine MI.
Why the study?
Does glucose-KCl-insulin solution improve oxidative phosphorylation and electrocardiographic abnormalities in dogs with experimentally induced myocardial infarction?
Does glucose-KCl-insulin solution improve oxidative phosphorylation and electrocardiographic abnormalities in dogs with experimentally induced myocardial infarction?
Answers are grounded in this paper and cite their sources.
Glucose-insulin-potassium (GIK) solution preserves mitochondrial oxidative phosphorylation and improves ECG abnormalities in a canine model of acute myocardial infarction.
Myocardial infarction was produced in dogs by ligature of the anterior descending coronary artery. Sarcosomes were isolated from normal and infarcted tissue. Oxygen consumption was followed polarographically and adenosine triphosphate was measured as glucose 6-phosphate. One group of animals received a continuous infusion of glucose for 12 hr; another group received "polarizing solution" (glucose-KCl-insulin). Sarcosomes from the first had a low oxygen consumption, no respiratory control, and no oxidative phosphorylation. In contrast, the administration of glucose-KCl-insulin solution maintained practically within normal limits these functional aspects of the sarcosomes. The reversal of electrocardiographic abnormalities by the administration of the polarizing solution coincided with improvement of such biochemical functions. Anesthesia and surgical handling did not appear to modify the behavior of the sarcosomes.
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Calva et al. (1965) studied Myocardial infarction. Glucose-KCl-insulin solution vs. Continuous infusion of glucose was evaluated on Oxygen consumption, respiratory control, and oxidative phosphorylation in sarcosomes. Administration of a glucose-KCl-insulin solution maintained normal oxygen consumption, respiratory control, and oxidative phosphorylation in sarcosomes of dogs with induced myocardial infarction.
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