| Autor(es): |
Prado, C. M.
;
Rossi, M. A.
;
Kimchi, A
Número total de Autores: 3
|
| Tipo de documento: | Artigo Científico |
| Fonte: | ADVANCES IN HEART DISEASE; v. N/A, p. 4-pg., 2006-01-01. |
| Resumo | |
The present investigation was carried out to elucidate the relationship between local hemodynamic forces and intimal and medial remodeling in the proximal and distal segments of the arterial walls of rats in relation to severe infradiaphragmatic stenosis of the aorta. Constricted aortas showed two distinct adaptive remodeling responses to hemodynamic stimuli induced by infradiaphragmatic coarctation. The first is remodeling in the hypertensive prestenotic segment with increased circumferential wall tension associated with normal tensile stress, laminar flow/normal wall shear stress characterized by enlarged heterogeneous endothelial cells, elongated in the direction of the blood flow, diffusely distributed neointimal plaques, appearing as discrete bulging toward the vascular lumen, and medial thickening. Our findings suggest that increased circumferential wall tension due to hypertension play a pivotal role in the remodeling of the prestenotic segment through biomechanical effects on oxidative stress and increased TGF-beta expression. The second is remodeling in the normotensive poststenotic segment with turbulent flow/low wall shear stress and normal circumferential wall tension and tensile stress characterized by groups of endothelial cells with phenotypic alterations and focally distributed neointimal plaques, similar but many of them larger than those found in the prestenotic segments. Further studies are needed to determine how the mechanical forces of turbulent flow/low shear stress are detected and transduced into chemical sign (s) by the cells of the artery walls and then converted into pathophysiologic relevant phenotypic changes. (AU) | |
| Processo FAPESP: | 04/14578-5 - Sepsis e choque septico: alteracoes funcionais e morfologicas do coracao. estudo experimental em camundongos. |
| Beneficiário: | Marcos Antonio Rossi |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |