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Published on: July 26, 2018
Prevention of myocardial generation in hamsters with hereditary cardiomyopathy
Abstract:
A number of drugs have been tested for their ability to prevent or change the course of skeletal and heart lesions occurring with a 100% incidence in cardiomyopathic hamsters (UM-X7.1). These drugs were selected because they act either on the metabolism or turnover of Ca or on adrenergic receptors. Verapamil (Isoptin), a potent inhibitor of myocardial transmembrane Ca conductivity, was found to completely prevent the myocardial lesions in myopathic hamsters. The hamsters were 28 to 30 days of age at the beginning of the experiment and were injected subcutaneously twice daily during 30 consecutive days in doses of 0.5 mg during the first week and 0.75 mg during the subsequent weeks. The protection afforded by Verapamil was no longer evident 30 days after interruption of the treatment. The severity of both cardiac and skeletal muscle lesions was found significantly lowered in hamsters receiving Dibenamine. It is assumed that Verapamil acts mainly by preventing excessive calcium influx in cardiomyocytes, whereas Dibenamine improves the microcirculation, which is deficient during the necrotizing phase of the polymyopathy. The latter assumption rests on the fact that, in myopathic hamsters, the reactivity pattern of alkaline phosphatase is altered at the level of the capillaries of cardiac and skeletal muscles.
Insights
Verapamil completely prevented heart lesions in cardiomyopathic hamsters by inhibiting calcium influx. Dibenamine also lowered lesion severity, potentially by improving microcirculation in this genetic cardiomyopathy model.
Area of Science:
- Cardiology
- Pharmacology
- Genetics
Background:
- Inherited cardiomyopathies in UM-X7.1 hamsters exhibit 100% incidence of skeletal and cardiac lesions.
- These lesions are associated with altered calcium (Ca) metabolism and adrenergic receptor activity.
Purpose of the Study:
- To evaluate the efficacy of Verapamil and Dibenamine in preventing or altering skeletal and heart lesions in cardiomyopathic hamsters.
- To investigate the mechanisms of action for Verapamil (calcium channel blockade) and Dibenamine (microcirculation improvement).
Main Methods:
- Myopathic hamsters (UM-X7.1) aged 28-30 days received daily subcutaneous injections of Verapamil or Dibenamine for 30 days.
- Verapamil doses were 0.5 mg/day for the first week, then 0.75 mg/day.
- Lesion severity and capillary alkaline phosphatase activity were assessed.
Main Results:
- Verapamil completely prevented myocardial lesions in treated hamsters.
- The protective effect of Verapamil was lost 30 days after treatment cessation.
- Dibenamine significantly reduced the severity of both cardiac and skeletal muscle lesions.
Conclusions:
- Verapamil's efficacy suggests a critical role for transmembrane calcium influx in myopathic hamster cardiomyopathy.
- Dibenamine's effects may stem from improved microcirculation, indicated by altered capillary alkaline phosphatase reactivity.
- These findings offer insights into potential therapeutic strategies for genetic cardiomyopathies.
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