Effects of enalapril on the collagen matrix in cardiomyopathic Syrian hamsters (BIO 14.6 and 53.58)

Kazuhiro Masutomo, Naoki Makino, Toru Maruyama, Tatsuo Shimada, Takashi Yanaga

    Research output: Contribution to journalArticlepeer-review

    7 Citations (Scopus)


    The hereditary cardiomyopathic strain of Syrian hamster has been extensively studied as a model of cardiomyopathy and heart failure. We attempted to determine whether an angiotensin converting enzyme (ACE) inhibitor, enalapril, prevents the increase in extracellular collagen matrix which connects the myocytes in cardiomyopathy. Enalapril was administered at an average dosage of 10 mg/kg per day to 10- to 20-week-old hamsters with hypertrophic (Bio 14.6) and dilated (Bio 53.58) cardiomyopathy, as well as to control Syrian hamsters (F1β). Collagen concentration estimated by hydroxyproline concentration and the collagen type III:I ratio significantly increased in the hearts of the Bio 14.6 and Bio 53.58 strains at 20 and 40 weeks of age as, compared with those in age-matched F1β hamsters. When Bio 14.6 hamsters were given enalapril for 10 weeks from 10 to 20 weeks of age, the collagen concentration, the collagen type III:I ratio and type III collagen mRNA expression were significantly decreased, compared with those in untreated animals of the same strain. After the administration of enalapril, scanning electron microscopic examination also revealed a decrease in fibrillar collagen accumulation in the interstitium and the network surrounding the cardiac myocytes. These prophylactic effects were not observed in the Bio 53.58 strain. These results indicate that the administration of ACE inhibitor prevents type III collagen production in the Bio 14.6 strain but not in the Bio 53.58 strain of Syrian hamster.

    Original languageEnglish
    Pages (from-to)50-61
    Number of pages12
    Issue number1
    Publication statusPublished - 1996

    All Science Journal Classification (ASJC) codes

    • Physiology
    • Cardiology and Cardiovascular Medicine


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