Document Detail


Characterization of an animal model of postmenopausal cardiac hypertrophy and novel mechanisms responsible for cardiac decompensation using ovariectomized pressure-overloaded rats.
MedLine Citation:
PMID:  19741553     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: The development of animal models of cardiovascular disease are critical to define pathophysiological mechanisms and to advance diagnosis and therapy. The lack of a suitable animal model represents a failure to define the mechanisms responsible for postmenopausal myocardial hypertrophy in hypertension and adverse cardiac remodeling. METHODS: In this review, we presented a rat model of postmenopausal myocardial hypertrophy, with particular focus on the similarities between the animal model and postmenopausal women regarding myocardial function as well as molecular and subcellular mechanisms. To elucidate the molecular mechanism of left ventricular (LV) hypertrophy and remodeling in postmenopausal women, we analyzed myocardial hypertrophy as well as cardiac function and hypertrophy-related protein expression in ovariectomized (OVX) and pressure overloaded (PO) rats. RESULTS: The model is characterized by depletion of serum estrogen and increased heart-to-body weight and lung-to-body weight ratios. Moreover, the OVX-PO rats also show increased mean arterial blood pressure, LV end-diastolic pressure, LV developed pressure, and maximal rates of LV contraction and relaxation compared with the OVX group. Importantly, Akt activity was largely attenuated, and both endothelial nitric oxide synthase expression and activity were markedly reduced in the OVX-PO group. Finally, significant increased mortality was observed in the OVX-PO group after chronic isoproterenol administration. CONCLUSIONS: Our results demonstrate that rats subject to OVX are unable to compensate for hypertrophy partly due to impaired Akt-endothelial nitric oxide synthase signaling along with deteriorated heart function and demonstrated increased mortality. In this review, we discussed the mechanisms of cardiac injury, which could play a critical role in postmenopausal hypertrophy, as well as the characteristics of the OVX-PO female rats as a model to test cardioprotective drugs in postmenopausal women.
Authors:
Md Shenuarin Bhuiyan; Kohji Fukunaga
Related Documents :
16824993 - Left ventricular chamber and myocardial systolic function reserve in patients with type...
15949473 - Additive amelioration of left ventricular remodeling and molecular alterations by combi...
8154493 - Detection of hemodialysis access outlet stenosis by measuring outlet resistance.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Menopause (New York, N.Y.)     Volume:  17     ISSN:  1530-0374     ISO Abbreviation:  Menopause     Publication Date:    2010 Jan-Feb
Date Detail:
Created Date:  2010-01-13     Completed Date:  2010-05-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9433353     Medline TA:  Menopause     Country:  United States    
Other Details:
Languages:  eng     Pagination:  213-21     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase
Animals
Disease Models, Animal*
Estrogens / blood
Female
Heart Failure / physiopathology
Hypertension
Hypertrophy, Left Ventricular / blood,  physiopathology*
Ovariectomy
Postmenopause / physiology*
Proto-Oncogene Proteins c-akt
Rats
Signal Transduction
Ventricular Remodeling / physiology
Chemical
Reg. No./Substance:
0/Estrogens; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Acidic catalase in human skin in vivo: a new marker of permanent damage.
Next Document:  Donald R. Korb, OD, FAAO: Clinician Scientist, Colleague, and Teacher.