title: Myocyte morphological characteristics differ between the phases of pulmonary hypertension-induced ventricular hypertrophy and failure.
abstract: Pulmonary hypertensive model rats were prepared by treating them with monochrotaline (MCT). Using these model rats, we examined myocyte remodeling in the right ventricle in response to increased right ventricular pressure. Male Sprague-Dawley rats were divided into 2 groups. Group M received MCT and group C received physiological saline. The 2 groups were examined at weeks 2, 5, and 7 after MCT or saline injection, respectively. At week 2, a significant difference in cell form was not observed in either group. At week 5, cell volume and myocyte cross-sectional area (CSA) of the right ventricle in group M were significantly greater than those in group C. At week 7, cell volume, CSA, and cell length of the right ventricle in group M were all significantly greater than those in group C. These results suggest that pulmonary hypertension causes hypertrophy, accompanying the enlargement of CSA in the right ventricle, and that cells lengthen in the phase of right ventricular failure. These results are similar to the changes observed in left ventricular myocytes due to overload pressure. Both right and left ventricular myocytes may share a common mechanism for myocyte remodeling as an adaptive and maladaptive response to increased ventricular pressure.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
authors.forename: Shunrou
authors.initials: S
authors.lastname: Minami
authors.forename: Tatsuyuki
authors.initials: T
authors.lastname: Onodera
authors.forename: Fumiko
authors.initials: F
authors.lastname: Okazaki
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Miyazaki
authors.forename: Shingo
authors.initials: S
authors.lastname: Ohsawa
authors.forename: Seibu
authors.initials: S
authors.lastname: Mochizuki
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D006333:Heart Failure / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000150:complications* / Q000473:pathology; D008297:Male; D016686:Monocrotaline / Q000633:toxicity; D032342:Muscle Cells / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D011379:Prognosis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D017725:Ventricular Pressure / Q000502:physiology; D020257:Ventricular Remodeling
chemical_list: D016686:Monocrotaline