Topic
Pulsatile flow
About: Pulsatile flow is a research topic. Over the lifetime, 6278 publications have been published within this topic receiving 149638 citations.
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TL;DR: The results suggest that the interstitial fluid flow is unlikely to cause the periosteal bone formation in venous stasis.
65 citations
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TL;DR: In this paper, the bi-viscosity model is used as a constitutive equation for blood, and the flow is assumed to be periodic, incompressible and axisymmetric.
65 citations
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TL;DR: The theory of dynamic fluid motion involving the forces manifested by mass, acceleration, viscous friction and vessel wall tension have been considered and studied when arterial blood flow and pressure are pulsatile and it is concluded that arterials blood pressure is dependent upon all of these parameters.
Abstract: The theory of dynamic fluid motion involving the forces manifested by mass, acceleration, viscous friction and vessel wall tension have been considered and studied when arterial blood flow and pressure are pulsatile. These studies and considerations have resulted in the conclusion that arterial blood pressure is dependent upon all of these parameters and that the relationship of pressure and flow is more complex and nonlinear than heretofore generally believed.
65 citations
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TL;DR: If hemodynamic factors play an important role in the problems of atherosclerosis, then, for macrocirculation studies, it is necessary to take into account unsteadiness and, in particular, the actual shape of the flow-time forcing function.
65 citations
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TL;DR: Pulsatile stretch activates ERK1/2 in the arterial wall via pathways different from those induced by steady overstretch, and levels in freshly isolated vessels were equivalent to the levels found in pulsatile vessels.
Abstract: Increased steady intraluminal pressure in blood vessels activates the extracellular signal-regulated kinase (ERK)1/2 pathway. However, signal transduction of pulsatile stretch has not been elucidated. Using an organ culture model of rabbit aorta, we studied ERK1/2 activation by pulsatility in vessels maintained at 80 mm Hg for 24 hours. ERK1/2 activity was evaluated by in-gel kinase assays and by Western blot. Compared with control aortas without pulsatility, aortas submitted to a pulsatile 10% variation in vessel diameter displayed a significant increase in ERK1/2 activity (207+/-12%, P<0.001), which remained high after removal of the endothelium. Unlike steady overstretch, pulsatile stretch-induced activation of ERK1/2 was not modified by herbimycin A, a Src family tyrosine kinase inhibitor, but was reduced by other tyrosine kinase inhibitors, tyrphostin A48 and genistein (162+/-27% and 144+/-14%, respectively). Conversely, ERK1/2 activity was markedly decreased in pulsatile vessels treated with staurosporine (114+/-18%) although neither of the more specific protein kinase C inhibitors, Ro-31-8220 or Go-6976, blocked ERK1/2 activation (209+/-24% and 238+/-34%, respectively), whereas staurosporine had no effect on steady overstretch-induced ERK1/2 activation. Pulsatility induced superoxide anion generation, which was prevented by the NADPH oxidase inhibitor diphenyleneiodonium. Furthermore, polyethylene glycol-superoxide dismutase completely abolished ERK1/2 activation by pulsatility (114+/-12%). Finally, ERK1/2 and O(2)(-) levels in freshly isolated vessels were equivalent to the levels found in pulsatile vessels. In conclusion, pulsatile stretch activates ERK1/2 in the arterial wall via pathways different from those induced by steady overstretch. Pulsatility might be considered a physiological stimulus that maintains a certain degree of ERK1/2 activation via oxygen-derived free radical production.
65 citations