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Prevention by cromakalim of spontaneously occurring cardiac necroses in polymyopathic hamsters
1Département de Pathologie, Université de Montréal, Québec, Canada.
Insights
Chronic treatment with cromakalim, a K+ ATP channel opener, significantly reduced heart necrosis in hereditary cardiomyopathy hamsters. This suggests potential cardioprotective benefits for this class of drugs in treating heart disease.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Hereditary cardiomyopathy in hamsters is linked to defective transmembrane ion flux and myocardial calcium overload.
- Potassium ATP (K+ ATP) channel openers have demonstrated efficacy in preventing calcium accumulation in ischemic heart conditions.
Purpose of the Study:
- To investigate the potential cardioprotective effects of chronic cromakalim (CR) treatment on the development of necrotic changes in hamster myopathic hearts.
Main Methods:
- Young cardiomyopathic (CM) hamsters received parenteral treatment with cromakalim (2.5 mg/kg/injection) twice daily for four weeks.
- Microscopic examination of serial paraffin sections of heart ventricles, diaphragm, and tongue tissues was performed at autopsy.
- Comparison of necrotic changes between CR-treated and control untreated hamsters.
Main Results:
- CR treatment significantly reduced necrotic calcific foci in hamster hearts compared to controls (p < 0.0001).
- Only minor myolytic lesions were observed in 5 out of 12 CR-treated hamsters.
- A significant reduction in the severity of the dystrophic process in the tongue was also noted in CR-treated animals (p < 0.0004).
Conclusions:
- Sustained in vivo treatment with a K+ ATP channel opener, cromakalim, demonstrates cardioprotection against the development of hereditary cardiomyopathy in hamsters.
- These findings suggest a therapeutic potential for K+ ATP channel openers in managing hereditary heart muscle diseases.
Abstract:
Previous studies on the heart necrotizing process at early stages of the hamster polymyopathy have led us to believe that this hereditary disease derives from a defective transmembrane ion flux resulting in myocardial Ca2+ over-load. On the other hand, certain K+ ATP channel openers were shown to prevent cytosolic Ca2+ accumulation in ischemic hearts. Therefore, we investigated the potential beneficial effect of chronic treatment with cromakalim (CR) on the development of necrotic changes in hamster myopathic hearts. Young cardiomyopathic (CM) hamsters were treated parenterally with CR over 4 consecutive weeks. The K+ ATP opener was dissolved in 5% DMSO and injected twice daily (s.c. and i.p. alternatively) at a dose level of 2.5 mg/kg per injection. Microscopic readings were carried out in staged serial paraffin sections of heart ventricles, the diaphragm, and tongue, will all tissues freshly taken at autopsy. In comparison with control untreated hearts, which exhibit numerous necrotic calcific foci, only minute myolytic lesions were found in 5 of 12 hamsters hearts receiving CR (p < 0.0001). Interestingly, the dystrophic process in the tongue was significantly less severe (p < 0.0004) in CR-treated animals. These observations provide evidence for the first time that in vivo sustained treatment with a K+ ATP opener exerts cardioprotection upon development of the hamster hereditary cardiomyopathy.