Abstract
Impairment of coronary flow, or low coronary reflow, is an important feature of ischemia-reperfusion injury. It is known to be associated with a significant diminution of basal and stimulated release of nitric oxide. The degree of recovery of low coronary reflow and of basal and stimulated release of nitric oxide diminishes with age and is influenced by the type of cardioplegic solution used. Underlying mechanisms include L-arginine (the physiologic substrate of nitric oxide) deficiency, G protein alteration, and nitric oxide inhibition by free radicals. Under normal conditions, basal release of nitric oxide is known to play a crucial role in the maintenance of basal coronary flow and appears to be essential for sustaining mechanical activity. Methods of preservation targeting reperfusion, ischemia, and preischemia have been evaluated. Pharmacologic modulation, crystalloid solution at 4 degrees C, and induction of heat-shock proteins (an intrinsic protective mechanism) reverse the postischemic dysfunction of nitric oxide release.
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