Under normal conditions, the heart is well oxygenated and consumes energy at a high rate. A nearly constant level of metabolites in the cytosol is maintained in myocardial cells via a balance between energy supply and expenditure. This balance is disrupted, however, in the ischemic setting. During ischemia, cardiac oxygen demand exceeds supply, resulting in decreased levels of high-energy phosphates, including phosphocreatine and adenosine triphosphate. In addition, increased free fatty acid levels inhibit glucose oxidation. Fatty acids, which produce less energy per unit of oxygen consumed compared to glucose, are used as fuel, and glucose metabolism is inhibited at the lactate step. Glycolysis in the absence of glucose oxidation increases lactate levels and intracellular acidosis. Prolonged or severe ischemia is associated with irreversible damage to mitochondrial membrane function and myocardial cell death. Mechanisms underlying these changes involve alterations in intracellular ion concentrations and mitochondrial damage. Metabolic changes in the heart during both short and prolonged ischemic conditions highlight the need for interventions aimed at preventing or reversing the cascade of events that result in cardiac cell death. Reperfusion of the ischemic myocardial tissue is beneficial in terms of potential recovery; however, myocytes alive at the time of reperfusion may become injured due to events initiated during reperfusion. Although not fully understood, reperfusion injury is a multifactorial process and affects various aspects of myocardial function. Production of oxygen free radicals and activation of polymorphonuclear leakocytes are hypothesized contributors to myocardial reperfusion injury. Biochemical changes in cardiac metabolism resulting from ischemia as well as consequences of reperfusion are reviewed.
|Original language||English (US)|
|Journal||Advanced Studies in Medicine|
|Issue number||6 B|
|State||Published - Jun 1 2004|
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