The mechanobiology of pulmonary vascular remodeling in the congenital absence of eNOS.
Biomech Model Mechanobiol
; 5(4): 217-25, 2006 Nov.
Article
em En
| MEDLINE
| ID: mdl-16520964
ABSTRACT
Primary pulmonary hypertension is a rare but deadly disease. Lungs extracted from PPH patients are deficient in endothelial nitric oxide synthase (eNOS), making the eNOS-null mouse a potentially useful model of the disease. To better understand the progression of pulmonary vascular remodeling in the congenital absence of eNOS, we induced pulmonary hypertension in eNOS-null mice using hypobaric hypoxia, and then quantified large artery structure and function in contralateral vessels. In particular, to assess structure we quantified diameter, wall thickness, and collagen, elastin and smooth muscle cell content; to quantify function we performed pressure-diameter tests. After remodeling, the pulmonary arteries had increased wall, collagen and elastin thicknesses compared to controls (P<0.05). The remodeled pulmonary arteries also had increased elastic moduli at low and high strains compared to controls (P<0.05). The increases in moduli at low and high strain correlated with increases in elastin and collagen thickness, respectively (P<0.05). These results provide insight into the mechanobiology of pulmonary vascular remodeling in the congenital absence of eNOS, and the coupled nature of these changes.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Óxido Nítrico Sintase Tipo III
/
Pulmão
/
Hipóxia
/
Músculo Liso Vascular
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Biomech Model Mechanobiol
Assunto da revista:
ENGENHARIA BIOMEDICA
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Estados Unidos