Energy metabolism in the hypertrophied heart.

摘要: In response to a prolonged pressure- or volume-overload, alterations occur in myocardial fatty acid, glucose, and glycogen metabolism. Oxidation of long chain acids has been found be reduced hypertrophied hearts compared non-hypertrophied hearts. However, this observation depends upon the degree cardiac hypertrophy, severity carnitine deficiency, concentration acid blood perfusate, workload. Glycolysis exogenous glucose is accelerated Despite acceleration glycolysis, oxidation not correspondingly increased leading lower coupling between glycolysis greater H+ production than Although metabolism does differ absence ischemia, synthesis degradation are severely ischemic These carbohydrate may contribute susceptibility injury during ischemia reperfusion by causing disturbances ion homeostasis that reduce contractile function efficiency extent normal. As hearts, pharmacologic enhancement (e.g., directly stimulating oxidation) improves recovery after ischemia. This provides strong support for concept modulation energy heart useful approach improve reperfusion. Future investigations necessary determine if alternative approaches, such as glucose-insulin-potassium infusion inhibitors ranolazine, trimetazidine), also produce beneficial effects reperfused