In a canine model, coronary ischemia shifts myocardial metabolism toward glycogenolysis and anaerobic glycolysis, particularly in the subendocardial layer.
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Animal data on subendocardial glycolysis in ischemia should not change practice; leaves open translation to human therapies.
The uptake of circulating substrates, lactate, glucose and free fatty acids (FFA) has been investigated concurrently with the tissular contents of these principles and the glycogen and triglyceride stores in the dog heart in situ submitted to incomplete obstruction of left coronary bed. Transmural samples necessary for the repeated determination of tissular substrates were taken from left ventricular wall by means of a total cardiopulmonary by-pass system, then divided to allow the analysis separately in subendocardial and subepicardial layer. A 40 to 70% reduction in coronary blood flow gave rise to decrease or suppression of uptake of all the substrates or even to conversion of uptake into output. The modifications of uptake are chiefly related to the deficiency of breakdown by oxidation, though lessened in the case of FFA by incorporation into triglycerides and enhanced in the case of glucose by glycogenolysis. Glycogenolysis and consequent anaerobic glycolysis appear to be the main process available against the energy cellular defect linked with oxygen lack which affects notably more subendocardial than subepicardial layer.
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Andrieu et al. (1981) studied this question.
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