Maintenance of intracellular homeostasis with respect to Ca++ during prolonged episodes of ischaemia and upon reperfusion is critical to the survival of the myocardium. Loss of Ca++ homeostasis results in massive ultrastructural damage, associated with excessive phospholipase and proteinase activation. Aggravating factors include hyperthermia, excessive cardiac work and hyperthyroidism. Conversely hypothermia, a reduction in sympathetic drive and a diminution in work load are all protective. Since the release of intracellular constituents, including enzymes and myoglobin, into the extracellular phase during post ischaemic reperfusion occurs as a secondary response to the Ca2+-induced tissue damage the quantitation of protective procedures that are based simply on the measurement of serum enzymes may not provide an accurate assessment of the degree of protection that has been achieved. In some instances it is possible to dissociate the gain in tissue Ca2+ from the release of intracellular constituents into the extracellular phase.
KeywordsSarcoplasmic Reticulum Mechanical Function Potassium Alteration Membrane Defect Protective Procedure
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