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Preservation of adenosine 5'-triphosphate and mitochondrial function during hypercalcemic reperfusion using verapamil
D R Jones1, A E Abbott, R C Hill
1Department of Surgery, West Virginia University, Morgantown.
Insights
Verapamil cardioplegia preserves myocardial adenosine triphosphate (ATP) stores and mitochondrial function during hypercalcemic reperfusion. However, it does not improve postischemic ventricular dysfunction.
Area of Science:
- Cardiology
- Cardiovascular Surgery
- Biochemistry
Background:
- Immediate hypercalcemic reperfusion can cause ventricular dysfunction and deplete myocardial energy stores.
- Maintaining myocardial energy during reperfusion is critical for cardiac function recovery.
Purpose of the Study:
- To assess the impact of verapamil cardioplegia on myocardial energy preservation, mitochondrial integrity, and ventricular function.
- To investigate the effects of verapamil during immediate hypercalcemic reperfusion in a rat heart model.
Main Methods:
- Rats received cardioplegia with potassium (control) or verapamil.
- Groups underwent either normocalcemic or hypercalcemic reperfusion.
- Adenosine triphosphate (ATP) levels, mitochondrial ultrastructure, and hemodynamic parameters were analyzed.
Main Results:
- Verapamil cardioplegia maintained ATP stores above 100% of control levels.
- No irreversible mitochondrial damage was observed with verapamil.
- Verapamil treatment resulted in significantly depressed heart rate, aortic flow, and dP/dT.
Conclusions:
- Verapamil cardioplegia protects myocardial ATP and mitochondrial function during immediate hypercalcemic reperfusion.
- Verapamil does not enhance postischemic hemodynamic recovery in this model.
- Further research may explore strategies to mitigate the negative hemodynamic effects of verapamil while retaining its protective benefits.
Abstract:
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 postischemic hemodynamics.