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Ann Thorac Surg 1991;51:705-710
© 1991 The Society of Thoracic Surgeons

Articles

Effect of calcium chloride administration on the postischemic isolated rat heart

Albert Abbott, MD, Ronald Hill, MD*, Larry Shears, BS, Kay Beamer, MS, Robert Gustafson, MD, Gordon Murray, MD

Department of Surgery, West Virginia University Medical Center, Morgantown, West Virginia USA

* Address reprint requests to Dr Hill, Department of Surgery, Health Sciences Center North, West Virginia University, Morgantown, VW 26506.

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. Hearts treated with calcium early during reperfusion demonstrated more mitochondrial damage and decreased stores of adenosine triphosphate than those in which calcium administration was delayed. The data indicate that a period of normocalcemic reperfusion should precede calcium administration in the postischemic heart. Mitochondrial damage resulting in decreased synthesis of adenosine triphosphate is likely the cause of ventricular dysfunction associated with calcium administration in the postischemic heart.




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