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

Matsui, S (författare)
Fu, Michael, 1963 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Wallenberglaboratoriet,Institute of Internal Medicine,Wallenberg Laboratory
Hayase, M (författare)
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Katsuda, T (författare)
Yamaguchi, N (författare)
Teraoka, K (författare)
Kurihara, T (författare)
Takekoshi, N (författare)
Wakabayashi, H (författare)
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 (creator_code:org_t)
2000
2000
Engelska.
Ingår i: Journal of cardiovascular pharmacology. - 0160-2446. ; 36 Suppl 2
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

Nyckelord

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

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