title: Spontaneously occurring hypertrophic cardiomyopathy in the rat. II. Distribution of, and correlations between, various cardiac abnormalities in the WKY/NCrj and its related strains.
abstract: We performed gross-anatomic and histologic examinations quantitatively on 18 male and 30 female WKY/NCrj rats, and their 299 first generation off spring. The results were analyzed in comparison with those obtained from 3 other strains of rats. The offspring of the WKY rats showed various cardiac abnormalities quite similar to those in their parents. The cardiac abnormalities in the offspring of the WKY rats were: increased heart weight (in about 10%), left or right atrial hypertrophy (50%), disproportionate septal thickening (50%), small left ventricular cavity (40%), right ventricular hypertrophy (40%), abnormal fiber arrangement greater than 5% in either of the 3 ventricular walls (90%), myocardial fibrosis (70%), and abnormal location of arteries in the ventricular septum (30%). ECG findings of the WHY-F rats such as high QRS complexes and high T waves and axis deviation showed a high sensitivity and specificity in the diagnosis of marked cardiac hypertrophy. Another conspicuous histologic finding observed in the WKY hearts was that the continuity of the latitudinal fiber bundle of the ventricular septum with that of the left ventricular free wall, an important functioning unit for pressure generation in the left ventricle, was markedly disturbed in the area of junction between the 2 walls; the smaller the continuity, the greater the cardiac hypertrophy; the disadvantage of the discontinuity for the pressure generation may be related to the development of cardiac hypertrophy. Also examined were two strains of Wistar rats with the same origin as the WKY/NCrj. These rats also had gross-anatomic and histologic abnormalities of the heart quite similar to those in the 2 generations of WKY/NCrj rats, suggesting that a common factor related to the development of the abnormalities, probably a genetic predisposition, has been transmitted in these 3 strains.
authors.affiliation: Second Department of Anatomy, Kyoto Prefectural University of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kuribayashi
authors.forename: T
authors.initials: T
authors.lastname: Mizuta
authors.forename: K
authors.initials: K
authors.lastname: Shimoo
authors.forename: Y
authors.initials: Y
authors.lastname: Kubota
authors.forename: H
authors.initials: H
authors.lastname: Katsume
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ibata
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000235:genetics / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology; D004195:Disease Models, Animal; D004562:Electrocardiography; D004719:Endomyocardial Fibrosis / Q000473:pathology; D005260:Female; D006345:Heart Septal Defects, Ventricular / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains / Q000235:genetics*; D011921:Rats, Inbred WKY / Q000235:genetics*; D013045:Species Specificity