Vessel Wall Hypertrophy
Mostrando 1-9 de 9 artigos, teses e dissertações.
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1. Estudo morfoquantitativo da parede da parte ascendente da aorta de ratos wistar idosos treinados em natação na intensidade do limiar de lactato
O envelhecimento está associado à elevação da pressão arterial sistólica, ao aumento da parede do ventrículo esquerdo e também, a uma maior rigidez na túnica íntima e média das artérias devido a diferentes fatores, como a destruição das fibras elásticas. Como forma de prevenir doenças cárdio - vasculares, promover mudanças na estrutura das
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 05/12/2011
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2. Alterações morfologicas e atividades e expressão de citocromos P450 no figado de ratos tratados com L-NAME / Hepatic morphological alterations and cytochrome P450 activities and expression in rats treated with L-NAME
Nitric oxide (NO), a co-product of the metabolism of L-arginine to L-citrulline by NO synthases (NOS), has an important role in regulating vascular tone, inflammatory responses, and the gene expression and enzymatic activity of various proteins, including cytochrome P450 and NOS. The chronic inhibition of NOS by Nffi-nitro-L-arginine methyl ester (L-NAME) pr
Publicado em: 2006
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3. Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia
Chronic hypoxia causes pulmonary hypertension with smooth muscle cell proliferation and matrix deposition in the wall of the pulmonary arterioles. We demonstrate here that hypoxia also induces a pronounced inflammation in the lung before the structural changes of the vessel wall. The proinflammatory action of hypoxia is mediated by the induction of distinct
The National Academy of Sciences.
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4. Wall thickness of coronary vessels varies transmurally in the LV but not the RV: implications for local stress distribution
Since the right and left ventricles (RV and LV) function under different loading conditions, it is not surprising that they differ in their mechanics (intramyocardial pressure), structure, and metabolism; such differences may also contribute to differences in the coronary vessel wall. Our hypothesis is that intima-media thickness (IMT), IMT-to-radius (IMT-to
American Physiological Society.
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5. Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells.
Recently, angiotensin II (Ang II) has been shown to cause hypertrophy of cultured quiescent rat aortic smooth muscle (RASM) cells. This observation along with the demonstration of angiotensinogen mRNA in the vessel wall has led us to postulate a role for vascular angiotensin in hypertensive blood vessel hypertrophy. To investigate further the possible molecu
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6. Blood pressure, flow, and peripheral resistance of digital arteries in vibration syndrome.
The peripheral circulation was studied in 19 lumberjacks and in 12 control subjects. Twelve of the lumberjacks were free from vascular symptoms and seven had vibration induced white finger (VWF). Using the strain-gauge plethysmographic technique, the digital circulation was examined at rest, during cooling of the upper body, and during heating of the upper b
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7. Evidence for direct local effect of angiotensin in vascular hypertrophy. In vivo gene transfer of angiotensin converting enzyme.
In vitro studies have demonstrated that angiotensin (Ang) II directly stimulates vascular smooth muscle cell (VSMC) growth. However, it is still unclear if Ang II exerts a direct effect on vascular hypertrophy in vivo independent of its effect on blood pressure. In vivo gene transfer provides the opportunity to assess the effects of increased activity of the
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8. Attenuated hypoxic pulmonary hypertension in mice lacking the 5-hydroxytryptamine transporter gene
Hypoxia is a well-recognized stimulus for pulmonary blood vessel remodeling and pulmonary hypertension development. One mechanism that may account for these effects is the direct action of hypoxia on the expression of specific genes involved in vascular smooth muscle cell (SMC) proliferation. Previous studies demonstrated that the serotonin (5-hydroxytryptam
American Society for Clinical Investigation.
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9. Pulmonary prostacyclin synthase overexpression in transgenic mice protects against development of hypoxic pulmonary hypertension
Prostacyclin synthase (PGIS) is the final committed enzyme in the metabolic pathway leading to prostacyclin (PGI2) production. Patients with severe pulmonary hypertension have a PGIS deficiency of their precapillary vessels, but the importance of this deficiency for lung vascular remodeling remains unclear. We hypothesized that selective pulmonary overexpres
American Society for Clinical Investigation.