Hypercalcemic reperfusion of the postischemic heart has been associated with ventricular dysfunction and with ultrastructural changes in the mitochondria. The isolated working rat heart model was used to correlate ventricular function, mitochondrial damage, and high-energy phosphate content with degree and timing of hypercalcemia during reperfusion. When administered early during reperfusion, calcium chloride caused a dose-dependent deterioration in ventricular function, whereas calcium augmented function when it was administered after a 15-minute period of normocalcemic reperfusion.
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