Summary
Reperfusion of calcium-deprived rat hearts with normal calcium-containing medium results in massive release of cell constituents, rapid depletion of tissue highenergy phosphate stores, and development of irreversible contracture (calcium paradox).
In an attempt to protect the heart against the calcium paradox, the slow channel calcium-antagonist drug verapamil (1 mg { litre-1) was added to the calcium-free medium and the reperfusion medium. Cell damage was quantitated in terms of creatine kinase (CK) release into the effluent medium, depletion of tissue creatine phosphate (CP) and adenosine triphosphate (ATP) stores, and development of contracture.
Verapamil did not reduce the initial rate of CK release from the hearts upon reperfusion with calcium-containing medium, but reduced the initial rate of myocardial CP and ATP depletion, and lessened the severity of the contracture.
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© 1980 Springer-Verlag Berlin-Heidelberg
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Ruigrok, T.J.C., Boink, A.B.T.J., Zimmerman, A.N.E., Meijler, F.L. (1980). Effect of Verapamil on Energy Consumption and Development of Contracture During the Calcium Paradox. In: Fleckenstein, A., Roskamm, H. (eds) Calcium-Antagonismus. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67595-9_14
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DOI: https://doi.org/10.1007/978-3-642-67595-9_14
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