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

Artikel i vetenskaplig tidskrift
Författare S Matsui
Michael Fu
M Hayase
T Katsuda
N Yamaguchi
K Teraoka
T Kurihara
N Takekoshi
H Wakabayashi
Publicerad i Journal of cardiovascular pharmacology
Volym 36 Suppl 2
Sidor S43-8
ISSN 0160-2446
Publiceringsår 2000
Publicerad vid Wallenberglaboratoriet
Institutionen för invärtesmedicin
Sidor S43-8
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Amino Acid Sequence, Angiotensin-Converting Enzyme Inhibitors, therapeutic use, Animals, Autoimmunity, Body Weight, drug effects, Cardiomyopathy, Dilated, drug therapy, etiology, Enzyme-Linked Immunosorbent Assay, Immunization, Lisinopril, blood, therapeutic use, Microscopy, Electron, Molecular Sequence Data, Myocardium, pathology, ultrastructure, Organ Size, drug effects, Rabbits, Receptors, Adrenergic, beta-1, immunology
Ämneskategorier Fysiologi, Cell- och molekylärbiologi

Sammanfattning

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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