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(Chest. 1995;107:307-310.)
© 1995 American College of Chest Physicians

Preservation of Adenosine 5'-Triphosphate and Mitochondrial Function During Hypercalcemic Reperfusion Using Verapamil Cardioplegia

David R. Jones MD1; Albert E. Abbott Jr. MD1; Ronald C. Hill MD1; Kay C. Beamer MS1; Robert A. Gustafson MD1; and Gordon F. Murray MD1

1 From the Department of Surgery, West Virginia University, Morgantown, WV.

Immediate hypercalcemic reperfusion results in ventricular dysfunction and loss of high-energy stores. The purpose of this study was to evaluate the effect of verapamil cardioplegia on the preservation of myocardial energy stores, mitochondrial ultrastructure, and ventricular dysfunction in the postischemic rat heart during immediate hypercalcemic reperfusion. Rats in the control group were subjected to cardioplegia with potassium, while rats in groups 1 to 3 were subjected to the same with verapamil (0.5 mg/L). The control and group 1 rats underwent normocalcemic reperfusion and groups 2 and 3 rats underwent hypercalcemic reperfusion. Myocardial samples were analyzed for adenosine 5'-triphosphate (ATP) content and mitochondrial ultrastructural damage. Hemodynamic parameters of heart rate, aortic flow (AF), and postischemic rate of aortic pressure change (dP/dT) also were evaluated. Data were analyzed using analysis of variance. The ATP stores were preserved at greater than 100% control levels in hearts subjected to verapamil cardioplegia. There was no evidence of irreversible mitochondrial damage. Heart rate, AF, and dP/dT were significantly (p<0.05) depressed in hearts subjected to verapamil cardioplegia. This study suggests verapamil cardioplegia preserves ATP and mitochondrial function during immediate hypercalcemic reperfusion but does not improve postis-chemic hemodynamics.

Key Words: adenosine 5'-triphosphate (ATP) preservation • hypercalcemic reperfusion • verapamil cardioplegia

Submitted on December 27, 1993
Accepted on April 26, 1994




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