Document Detail

Myocyte morphological characteristics differ between the phases of pulmonary hypertension-induced ventricular hypertrophy and failure.
MedLine Citation:
PMID:  16960417     Owner:  NLM     Status:  MEDLINE    
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.
Shunrou Minami; Tatsuyuki Onodera; Fumiko Okazaki; Hidekazu Miyazaki; Shingo Ohsawa; Seibu Mochizuki
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  International heart journal     Volume:  47     ISSN:  1349-2365     ISO Abbreviation:  -     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-09-08     Completed Date:  2007-10-16     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  101244240     Medline TA:  Int Heart J     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  629-37     Citation Subset:  IM    
Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
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MeSH Terms
Cardiomegaly / etiology,  pathology*,  physiopathology
Disease Models, Animal
Disease Progression
Heart Failure / etiology,  pathology*,  physiopathology
Hypertension, Pulmonary / chemically induced,  complications*,  pathology
Monocrotaline / toxicity
Muscle Cells / pathology*
Myocardium / pathology*
Rats, Sprague-Dawley
Severity of Illness Index
Ventricular Pressure / physiology
Ventricular Remodeling
Reg. No./Substance:

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