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Verapamil preserves adenine nucleotide pool in cardiomyopathic Syrian hamster
Insights
Calcium entry blockers like verapamil may preserve cardiac function and energy levels in heart failure. This study shows verapamil treatment improved high-energy phosphates and cardiac performance in cardiomyopathic hamsters.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Heart failure in cardiomyopathic Syrian hamsters shows decreased energy metabolism, including total adenine nucleotides and high-energy phosphates.
- This metabolic dysfunction correlates with reduced cardiac performance and oxygen consumption.
Purpose of the Study:
- To investigate the potential of calcium entry blockers to preserve cardiac energy metabolism and function during heart failure.
- To evaluate the effects of verapamil on adenine nucleotides and high-energy phosphates in a hamster model of cardiomyopathy.
Main Methods:
- Cardiomyopathic Syrian hamsters with heart failure were treated with verapamil in drinking water for two months prior to death.
- Cardiac performance, oxygen consumption, and levels of adenine nucleotides and high-energy phosphates (ATP/total ADP, PCr/Cr) were measured.
Main Results:
- Verapamil treatment preserved total adenine nucleotides, cyclic AMP (cAMP), and high-energy phosphates in cardiomyopathic hamsters.
- Cardiac performance and oxygen consumption were improved in verapamil-treated cardiomyopathic hamsters compared to untreated controls.
- Verapamil-treated cardiomyopathic hamsters showed preserved cardiac function, comparable to verapamil-treated healthy hamsters.
Conclusions:
- Calcium entry blockers, specifically verapamil, can improve cardiac performance and preserve critical energy metabolites during heart failure in this model.
- This study provides the first evidence that calcium entry blockers may offer a protective effect on cardiac energy status in the failing heart.
Abstract:
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.