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  • Matsui, S (author)

Beneficial effect of angiotensin-converting enzyme inhibitor on dilated cardiomyopathy induced by autoimmune mechanism against beta1-adrenoceptor.

  • Article/chapterEnglish2000

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  • 2000

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  • LIBRIS-ID:oai:gup.ub.gu.se/60167
  • https://gup.ub.gu.se/publication/60167URI

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  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • We have shown that a peptide corresponding to the sequence of the second extracellular loop of the human beta1-adrenoceptor (beta1-peptide) was able to induce an autoimmune cardiomyopathy in rabbits. In this study, we examined the effect of angiotensin-converting enzyme inhibitor (ACEI) on beta1-peptide-induced cardiomyopathy. Rabbits were divided into four groups: (1) control group (n= 6) receiving saline injection; (2) beta1-peptide group (n = 8) immunized with beta1-peptide; (3) ACEI group (n = 6), lisinopril (3 mg/day) given orally and receiving saline injection; and (4) ACEI + beta1-peptide group (n = 7), lisinopril (3 mg/day) given orally and immunized with beta1-peptide. Our results showed that, after 1 year, all rabbits in the beta1-peptide group had an increase in heart weight, wall thinning and dilatations of both ventricles as compared with rabbits in the ACEI + beta1-peptide group that had normal heart weight and shape. All rabbits in the beta1-peptide group exhibited multifocal degeneration and necrosis of myocardial cells with moderate infiltration of inflammatory cells. In the ACEI + beta1-peptide group, three rabbits showed focal degeneration and necrosis of myocardial cells accompanied by mononuclear cells. The lesions in this group were apparently less marked than those in the beta1-peptide group. In conclusion, ACEI protects the myocardium from injury induced by an autoimmune mechanism against beta1-adrenoceptor.

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  • Fu, Michael,1963Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Wallenberglaboratoriet,Institute of Internal Medicine,Wallenberg Laboratory(Swepub:gu)xfumiw (author)
  • Hayase, M (author)
  • Katsuda, T (author)
  • Yamaguchi, N (author)
  • Teraoka, K (author)
  • Kurihara, T (author)
  • Takekoshi, N (author)
  • Wakabayashi, H (author)
  • Göteborgs universitetInstitutionen för invärtesmedicin (creator_code:org_t)

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  • In:Journal of cardiovascular pharmacology36 Suppl 20160-2446

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