title: Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats.
abstract: Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.
authors.affiliation: 4th Department of Internal Medicine, Shimane Medical University, Izumo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Morioka
authors.forename: M
authors.initials: M
authors.lastname: Honda
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ishinaga
authors.forename: S
authors.initials: S
authors.lastname: Yano
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Moriyama
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D003094:Collagen / Q000378:metabolism*; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000150:complications; D008297:Male; D008855:Microscopy, Electron, Scanning; D008929:Mitochondria, Heart / Q000648:ultrastructure; D016686:Monocrotaline; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009218:Myosins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012519:Sarcoplasmic Reticulum / Q000648:ultrastructure
chemical_list: D016686:Monocrotaline; D003094:Collagen; D009218:Myosins; D002118:Calcium