Variation of the origin of aortic arch branches: in relationship with plates of atheroma / Variación del origen de las ramas del arco aórtico: relación con placas de ateromas

The aortic arch branches variations have called the attention of several authors, who have handled studies and classifications, both human and in different animals. The common trunk, which is between the brachiocephalic trunk and the common left carotid artery, is the most common variation. We conducted a descriptive and randomized study of the presence of the trunk mentioned before, trying to establish the possible relationship between this variation and the distribution plates of atheroma. The lumen observation makes it possible to define and check the distribution of the ostium, among the common ostium and the ones with common trunks. Regarding the plates of atheroma, it was found that there is a slight prevalence in common trunks cases, with respect to the classics (no variety) or the ones who had common ostium. In all cases, the presence of a plaque in the distal aortic arch was certified near the left subclavian artery. The knowledge of the existence of the common trunk sets up an act of academic interest, as practice interventions and diagnostic imaging and clinical work, since the presence of the common trunk might be related to the prevalence of the plates of atheroma at the level of its origin.

Las variaciones de las ramas del arco aórtico han llamado la atención de diversos autores, quienes han realizados estudios y clasificaciones, tanto en humanos, como en diferentes animales. El tronco común, entre el tronco braquiocefálico y la arteria carótida común izquierda, es la variación más frecuente. Realizamos un estudio descriptivo y randomizado de la presencia del mencionado tronco, tratando de verificar la posible relación entre dicha variación y la distribución de placas de ateroma. La observación luminal permitió precisar, entre los casos de ostios comunes y aquellos con troncos comunes, y comprobar la distribución de los ostios. En cuanto a las placas de ateroma, se observó una leve prevalencia en los casos de troncos comunes respecto de los clásicos (sin variedad) o de los que presentaron ostios comunes. En todos los casos se verificó la presencia de una placa en el arco aórtico distal, inmediato a la arteria subclavia izquierda. El conocimiento de la existencia del tronco común, constituye un hecho de interés académico, como práctico en intervencionismo, diagnóstico por imagen y la clínica. La presencia del tronco común pareciera estar relacionada con cierta prevalencia de placas de ateroma a nivel de su origen.

Shear stress stimulates phosphorylation of protein kinase A substrate proteins including endothelial nitric oxide synthase in endothelial cells

Fluid shear stress plays a critical role in vascular health and disease. While protein kinase A (PKA) has been implicated in shear-stimulated signaling events in endothelial cells, it remains unclear whether and how PKA is stimulated in response to shear stress. This issue was addressed in the present study by monitoring the phosphorylation of endogenous substrates of PKA. Shear stress stimulated the phosphorylation of cAMP responsive element binding protein (CREB) in a PKA-dependent manner. Western blot analysis using the antibody reactive against the consensus motif of PKA substrates detected two proteins, P135 and P50, whose phosphorylation was increased by shear stress. The phosphorylation of P135 was blocked by a PKA inhibitor, H89, but not by a phosphoinositide 3-kinase inhibitor, wortmannin. Expression of a constitutively active PKA subunit stimulated P135 phosphorylation, supporting the potential of P135 as a PKA substrate. P135 was identified as endothelial nitric oxide synthase (eNOS) by immunoprecipitation study. PKA appeared to mediate shear stress-stimulated eNOS activation. Shear stress stimulated intracellular translocation of PKA activity from 'soluble' to 'particulate' fractions without involving cellular cAMP increase. Taken together, this study suggests that shear stress stimulates PKA-dependent phosphorylation of target proteins including eNOS, probably by enhancing intracellular site-specific interactions between protein kinase and substrates.

Hiper-homocisteinemia causando aterogênese na aorta de coelhos: modelo experimental / Hyperhomocysteinemia causing atherogenesis in rabbits´aorta: an experimental model

Objetivo: Este estudo tem por objetivo avaliar os efeitos da homocisteinemia plasmática elevada na formação da placa aterosclerótica na aorta de coelhos. Material e método: Realizou-se estudo experimental comparativo em dois grupos homogêneos de coelhos durante 60 dias. Foram utilizados 20 coelhos da linhagem New Zealand divididos em dois grupos de 10 animais: grupo controle (C) e grupo metionina (M). Todos os animais receberam a mesma dieta sólida e 500 ml de água. Os animais do grupo M receberam 2 ml de uma solução de metionina na concentração de 200 mg/ml a cada 24 horas. Foram colhidas amostras de sangue para a dosagem de colesterol, triglicerídeos, HDL, LDL e homocisteína após 0, 30 e 60 dias. Os animais foram submetidos a eutanásia por dose letal de anestésico no 60° dia. A aorta torácica e a aorta abdominal foram retiradas para estudo anatomopatológico...

Inhibition of rac1 Reduces PDGF-induced Reactive Oxygen Species and Proliferation in Vascular Smooth Muscle Cells

In vascular smooth muscle cells, reactive oxygen species (ROS) were known to mediate platelet-derived growth factor (PDGF)-induced cell proliferation and NADH/NADPH oxidase is the major source of ROS. NADH/NADPH oxidase is controlled by rac1 in non-phagocytic cells. In this study, we examined whether the inhibition of rac1 by adenoviral-mediated gene transfer of a dominant negative rac1 gene product (Ad.N17rac1) could reduce the proliferation of rat aortic vascular smooth muscle cells (RASMC) stimulated by PDGF via decreasing intracellular ROS. RASMC were stimulated by PDGF (80 ng/mL) with or without N-acetylcysteine 1 mM or infected with 100 mutiplicity of infection of Ad.N17rac1. Intracellular ROS levels were measured at 12 hr using carboxyl-2', 7'-dichlorodi-hydrofluorescein diacetate confocal microscopy. At 72 hr, cellular proliferation was evaluated by cell number counting and XTT assay. Compared with control, ROS levels were increased by 2-folds by PDGF. NAC and Ad.N17rac1 inhibited PDGF-induced increase of ROS by 77% and 65%, respectively. Cell number was increased by PDGF by 1.6-folds compared with control. NAC and Ad.N17rac1 inhibited PDGF-induced cellular growth by 45% and 87%, respectively. XTT assay also showed similar results. We concluded that inhibition of rac1 in RASMCs could reduce intracellular ROS levels and cellular proliferation induced by PDGF.

Vascular smooth muscle cells cultured on elastin membranes

Smooth muscle cells from thoracic aortas of 12-week-old rats were cultured on elastin membranes for up to 21 days. The cell cultures were examined using light microscopy, trasmission and scanning electron microscopy. The contractile phenotype characteristic for resident arterial wall muscle cell changed to the synthetic phenotype. In the synthetic state, the muscle cells contain few filaments, but a substantial amount of orgenelles are involved with synthesis. The cells grown on elastin substrates showed a multilayered pattern with the formation of nodules. Cell degeneration was present from dayeight and increased with time. At the end of the experiment, the center of the multilayered areas showed degenerative changes with numerous foam cells of smooth muscle origin, areas of necrosis and a considerable amount of calcium deposit. Our experimental model would be valuable in the investigation of the pathological changes associated with smooth muscle cell proliferation in vessels