About: Pulsatile flow is a(n) research topic. Over the lifetime, 6278 publication(s) have been published within this topic receiving 149638 citation(s).
Papers published on a yearly basis
TL;DR: It is demonstrated that in addition to prostacyclin, flow triggers the release of another relaxing substance (or substances) from vascular endothelial cells that has characteristics similar to the endothelium-derived relaxing factor released by acetylcholine.
Abstract: To analyze the potential mediator(s) involved in flow-induced endothelium-dependent vasodilation, we measured the wall tension of intraluminally perfused canine femoral artery segments and compared the content of 6-ketoprostaglandin F1 alpha (determined by radioimmunoassay) and the relaxing activity of the effluent (determined by bioassay on canine coronary artery rings). During perfusion at a steady flow of 2 ml/min the effluent contained 6-keto-prostaglandin F1 alpha and relaxed the bioassay rings. Sudden increase in steady flow rate to 4 ml/min, or the introduction of pulsatile flow, increased the release of 6-keto-prostaglandin F1 alpha and induced further relaxations of the bioassay ring. No relaxations were observed with the effluent passing through a femoral artery segment without endothelium. Indomethacin significantly depressed the release of 6-keto-prostaglandin F1 alpha during increases in flow but had no significant effect on the relaxing activity of the effluent. In the presence of indomethacin, increases in flow produced significant relaxation in the perfused femoral artery segments with endothelium. Superoxide dismutase restored the relaxing activity of the effluent during increases in flow at a transit time of 30 seconds. These data demonstrate that in addition to prostacyclin, flow triggers the release of another relaxing substance (or substances) from vascular endothelial cells that has characteristics similar to the endothelium-derived relaxing factor released by acetylcholine.
TL;DR: The steady-state production rate of cells subjected to pulsatile shear stress was more than twice that of cells exposed to steadyShear stress and 16 times greater than that of Cells in stationary culture.
Abstract: Endothelial cell functions, such as arachidonic acid metabolism, may be modulated by membrane stresses induced by blood flow. The production of prostacyclin by primary human endothelial cell cultures subjected to pulsatile and steady flow shear stress was measured. The onset of flow led to a sudden increase in prostacyclin production, which decreased to a steady rate within several minutes. The steady-state production rate of cells subjected to pulsatile shear stress was more than twice that of cells exposed to steady shear stress and 16 times greater than that of cells in stationary culture.
TL;DR: The study of arterial blood flow will lead to the prediction of individual hemodynamic flows in any patient, the development of diagnostic tools to quantify disease, and the design of devices that mimic or alter blood flow.
Abstract: Blood flow in arteries is dominated by unsteady flow phenomena. The cardiovascular system is an internal flow loop with multiple branches in which a complex liquid circulates. A nondimensional frequency parameter, the Womersley number, governs the relationship between the unsteady and viscous forces. Normal arterial flow is laminar with secondary flows generated at curves and branches. The arteries are living organs that can adapt to and change with the varying hemodynamic conditions. In certain circumstances, unusual hemodynamic conditions create an abnormal biological response. Velocity profile skewing can create pockets in which the direction of the wall shear stress oscillates. Atherosclerotic disease tends to be localized in these sites and results in a narrowing of the artery lumen—a stenosis. The stenosis can cause turbulence and reduce flow by means of viscous head losses and flow choking. Very high shear stresses near the throat of the stenosis can activate platelets and thereby induce thrombosis, which can totally block blood flow to the heart or brain. Detection and quantification of stenosis serve as the basis for surgical intervention. In the future, the study of arterial blood flow will lead to the prediction of individual hemodynamic flows in any patient, the development of diagnostic tools to quantify disease, and the design of devices that mimic or alter blood flow. This field is rich with challenging problems in fluid mechanics involving three-dimensional, pulsatile flows at the edge of turbulence.
10 Jun 2003-Circulation
TL;DR: It appears likely that the totality of the BP curve, not simply 2 specific and arbitrary points, should be considered to act mechanically on the arterial wall and therefore should be used to propose an adequate definition of high BP.
Abstract: Blood pressure (BP) is a powerful cardiovascular (CV) risk factor that acts on the arterial wall and is responsible in part for various CV events, such as cerebrovascular accidents and ischemic heart disease. In clinical practice, 2 specific and arbitrary points of the BP curve, peak systolic BP (SBP) and end-diastolic BP (DBP), are used to define the CV risk factor. Because the goal of drug treatment of hypertension is to prevent CV complications, it appears likely that the totality of the BP curve, not simply 2 specific and arbitrary points, should be considered to act mechanically on the arterial wall and therefore should be used to propose an adequate definition of high BP. A current approach consists of considering the BP curve as the summation of a steady component, mean blood pressure (MBP), and a pulsatile component, pulse pressure (PP).1 MBP, the product of cardiac output multiplied by total peripheral resistance, is the pressure for the steady flow of blood and oxygen to peripheral tissues and organs. The pulsatile component, PP, is the consequence of intermittent ventricular ejection from the heart. PP is influenced by several cardiac and vascular factors, but it is the role of large conduit arteries, mainly the aorta, to minimize pulsatility. In addition to the pattern of left ventricular ejection, the determinants of PP (and SBP) are the cushioning capacity of arteries and the timing and intensity of wave reflections.1 The former is influenced by arterial stiffness, usually expressed in the quantitative terms of compliance and distensibility.1 The latter result from the summation of a forward wave coming from the heart and propagating at a given speed (pulse wave velocity, or PWV) toward the origin of resistance vessels and a backward wave returning toward the heart from particular sites characterized by specific …
01 May 1992-Circulation
TL;DR: The Doppler guide wire measures phasic flow velocity patterns and linearly tracks changes in flow rate in small, straight coronary arteries and should facilitate measurement ofphasic coronary flow velocity during coronary angiography and angioplasty.
Abstract: BACKGROUNDAn improved intravascular ultrasonic Doppler device could aid the clinical assessment of coronary hemodynamics. We evaluated a new device consisting of a 12-MHz piezoelectric transducer integrated onto the tip of a 0.018-in. flexible, steerable angioplasty guide wire.METHODS AND RESULTSDoppler spectra were recorded in model tubes with pulsatile blood flow and in-line electromagnetic flowmeter. In four straight tubes (i.d., 0.79-4.76 mm), the time average of spectral peak velocity (APV) was linearly related to blood flow (QEMF) (r2 greater than or equal to 0.98 for each tube). A Doppler-derived quantitative flow estimate (QD) was calculated as the product of vessel cross-sectional area and mean velocity, with mean velocity estimated as 0.5 x APV. The slope of QD versus QEMF for the four tubes was near unity. APV was less accurate in a 7.94-mm straight tube and in tortuous segments. In four dogs, the left circumflex coronary artery (LCx) was perfused from the femoral artery via a cannula with in-l...
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