Concept of Cardioprotection Against Myocardial Ischemia
When the oxygen supply to the myocardium is restricted by an occlusion or narrowing of the coronary artery, ischemic changes are induced and eventually irreversible injury occurs after some critical period of ischemia. To salvage the ischemic myocardium, early restoration of blood supply is most effective. Accumulating evidence, however, suggests that appropriate techniques of reperfusion may salvage more myocytes than the simple reperfusion since reperfusion itself may cause the additional irreversible injury.1 Accumulation of toxic substances such as hydrogen ions, lactate, fatty acid derivatives, free radicals and intracellular calcium overload may cause the transition from reversible to irreversible injury. Microvascular injuries during ischemia and reperfusion also accelerate the ischemic damage and disturb the restoration of blood perfusion after recanalization. Preservation of microvascular integrity and acceleration of collateral development are protective against the ischemic damage. Various interventions which could scavenge free radicals and inhibit calcium overload after reperfusion have been reported. During cardiac surgery cardioplegia are commonly used to protect the myocardium from the ischemic injury. In prophylactic view, acquisition of ischemic tolerance against irreversible injury is also important. Since certain stress such as brief reversible ischemia, hypoxia, heat and oxidative stress could render the heart tolerable against myocardial infarction and functional deterioration. Ischemic preconditioning could markedly attenuate infarct size and postischemic dysfunction and arrhythmia. A delayed protective action of ischemic preconditioning is also observed. Although the precise mechanisms of this phenomenon are not clarified yet, clinical application may provide a great benefit for patients with ischemic heart disease.
KeywordsIschemia Adenosine Catalase Thrombin Creatine
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