Why the study?
Does verapamil preserve adenine nucleotides and improve cardiac performance in cardiomyopathic Syrian hamsters with heart failure?
Does verapamil preserve adenine nucleotides and improve cardiac performance in cardiomyopathic Syrian hamsters with heart failure?
Verapamil preserves high-energy phosphates and cardiac performance in a hamster model of congestive heart failure.
Does not support verapamil use in human HF; hypothesis-generating for energetic effects in cardiomyopathy models.
There is a decrease in total adenine nucleotides, cyclic AMP (cAMP), ATP/total ADP, and phosphocreatine (PCr)/creatine (Cr) both in situ and in the perfused heart in the heart failure stage of the cardiomyopathic Syrian hamster. There were decreases in developed pressure, dP/dt, and O2 consumption associated with the decrease in total adenine nucleotides and cAMP. Cardiomyopathic Syrian hamsters (180-240 days old) with congestive heart failure were given water with the calcium entry blocker, verapamil, as an additive 2 mo before death. In the cardiomyopathic group given verapamil the adenine nucleotides, cAMP, and high-energy phosphates were preserved and cardiac performance was not significantly different from that of the verapamil-treated healthy hamsters at the time of death. Pretreatment of cardiomyopathic animals with verapamil (6.6 mg verapamil/ml water consumed by drinking) resulted in significantly higher ATP/total ADP and PCr/Cr compared with nontreated cardiomyopathic hamsters. This is the first report demonstrating that a calcium entry blocker may improve cardiac performance and preserve total adenine nucleotides during the heart failure stage of the cardiomyopathic hamster.
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Wikman‐Coffelt et al. (1986) studied this question.
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