Relations between myocardial contractility, myosin phenotype, and plasma angiotensin-converting enzyme activity in the cardiomyopathic hamster.
Angiotensin-converting enzyme (ACE) inhibitors have been shown to preserve myocardial contractility in the cardiomyopathic Syrian hamster (CSH). To determine if this was related to changes in myosin heavy-chain (MHC) phenotype, myosin isoform patterns and mechanical properties were studied in the same left ventricular papillary muscle from CSH of the Bio 53.58-dilated strain. From age 1 to 6 months, 22 CSH randomly received either perindopril 1 mg/kg/day in distilled water (PE, n = 11) or distilled water only (PL, n = 11), and seven control golden Syrian hamsters (C) received distilled water by force-feeding. Compared to C, PL had a lower Vmax (p < 0.01), a lower amount of alpha-MHC (p < 0.01), and an unchanged twitch duration. In PE, as compared to PL, there was a higher Vmax (p < 0.05), a higher alpha-MHC (p < 0.05), and an unchanged twitch duration. There was a positive relationship between Vmax and alpha-MHC in the population taken as a whole (p < 0.01), and when muscles from C and PL groups were plotted together (p < 0.001), but neither within each group, nor when PL and PE were plotted together. Our study indicates that in CSH (a) the preserved contractility with ACE-inhibitor treatment is associated with limitation of isomyosin shift induced by the myopathic process, but no cause-to-effect relationship could be demonstrated on the basis of our data, and (b) adaptive changes in twitch duration were not observed either in untreated CSH or in perindopril-treated CSH, despite significant changes in alpha-MHC content.
Lambert
F
F
INSERM U275-Loa-Ensta-Ecole Polytechnique, Palaiseau, France.
Lecarpentier
Y
Y
Lompré
A M
AM
Scalbert
E
E
Desché
P
P
Chemla
D
D
D000818:Animals; D009202:Cardiomyopathies / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology*; D006224:Cricetinae; D066298:In Vitro Techniques; D007536:Isomerism; D008297:Male; D008647:Mesocricetus; D009200:Myocardial Contraction / Q000187:drug effects*; D015879:Myosin Subfragments / Q000235:genetics / Q000378:metabolism; D009218:Myosins / Q000235:genetics*; D010210:Papillary Muscles / Q000187:drug effects; D007703:Peptidyl-Dipeptidase A / Q000097:blood*; D010641:Phenotype
D015879:Myosin Subfragments; D007703:Peptidyl-Dipeptidase A; D009218:Myosins