Pulsatile flow

About: Pulsatile flow is a research topic. Over the lifetime, 6278 publications have been published within this topic receiving 149638 citations.

Pulsatile Blood Flow

Abstract: Hence does arise the action and function of the heart, which by pulsation it performs. [William Harvey, De Motu Cordis, 1628.] THE study of blood flow as a pulsatile phenomenon is scarcely new, but it has gained new impetus from three recent developments: the commercial production of reliable blood flowmeters, the formulation of theories appropriate to oscillatory flow in blood vessels,1 and the increasing availability of digital computers. Studies in laboratory animals have profited from these technical advances for some time, and clinical investigation of pulsatile flow is now possible with catheter-tip flowmeters that can be used in routine cardiac . . .

Three-dimensional instabilities and transition of steady and pulsatile axisymmetric stenotic flows

Abstract: A straight tube with a smooth axisymmetric constriction is an idealized representation of a stenosed artery. We examine the three-dimensional instabilities and transition to turbulence of steady flow, steady flow plus an oscillatory component, and an idealized vascular pulsatile flow in a tube with a smooth 75 % stenosis using both linear stability analysis and direct numerical simulation. Steady flow undergoes a weak Coanda-type wall attachment and turbulent transition through a subcritical bifurcation, leading to hysteretic behaviour with respect to changes in Reynolds number. The pulsatile flows become unstable through a subcritical period-doubling bifurcation involving alternating tilting of the vortex rings that are ejected from the throat with each pulse. These tilted vortex rings rapidly break down through a self-induction mechanism within the confines of the tube. While the linear instability modes for pulsatile flow have maximum energy well downstream of the stenosis, we have established using direct numerical simulation that breakdown can gradually propagate upstream until it occurs within a few tube diameters of the constriction, in agreement with previous experimental observations. At the Reynolds numbers employed in the present study, transition is localized, with relaminarization occurring further downstream. A non-exhaustive investigation has also been undertaken into the receptivity of the axisymmetric shear layer in the idealized physiological pulsatile flow, with the results suggesting it has localized convective instability over part of the pulse cycle.

A new in vitro model to evaluate differential responses of endothelial cells to simulated arterial shear stress waveforms.

Abstract: In the circulation, flow-responsive endothelial cells (ECs) lining the lumen of blood vessels are continuously exposed to complex hemodynamic forces. To increase our understanding of EC response to these dynamic shearing forces, a novel in vitro flow model was developed to simulate pulsatile shear stress waveforms encountered by the endothelium in the arterial circulation. A modified waveform modeled after flow patterns in the human abdominal aorta was used to evaluate the biological responsiveness of human umbilical vein ECs to this new type of stimulus. Arterial pulsatile flow for 24 hours was compared to an equivalent time-average steady laminar shear stress, using no flow (static) culture conditions as a baseline. While both flow stimuli induced comparable changes in cell shape and alignment, distinct patterns of responses were observed in the distribution of actin stress fibers and vinculin-associated adhesion complexes, intrinsic migratory characteristics, and the expression of eNOS mRNA and protein. These results thus reveal a unique responsiveness of ECs to an arterial waveform and begin to elucidate the complex sensing capabilities of the endothelium to the dynamic characteristics of flows throughout the human vascular tree.

Pulmonary Vascular Impedance in the Dog

Abstract: Pulmonary vascular hydraulic input impedance was measured in 13 anesthetized openchest dogs with normal sinus rhythm, and 2 dogs with surgically induced atrioventricular block, by means of electromagnetic flowmeters and strain gauge manometers of known frequency response. The linearity of the pulmonary bed was evaluated by measuring impedance while the heart rate, and hence the pulsatile input to the bed, was varied. The pulmonary bed behaved as a quasilinear system, within the limits of accuracy of the methods employed and the range of frequencies tested. The use of input impedance, or oscillatory pressure/flow ratio, to describe some characteristics of the bed is therefore justifiable, and analogies with linear models like the simple transmission line are not unreasonable. The characteristic input impedance averaged 3,094 dyne sec cm-5 kg, or about one-third the magnitude of the pulmonary vascular resistance, and was therefore a significant part of the total opposition that must be overcome in moving bl...

Pulsatile Stretch Remodels Cell-to-Cell Communication in Cultured Myocytes

Abstract: Mechanical stretch is thought to play an important role in remodeling atrial and ventricular myocardium and may produce substrates that promote arrhythmogenesis. In the present work, neonatal rat ventricular myocytes were cultured for 4 days as confluent monolayers on thin silicone membranes and then subjected to linear pulsatile stretch for up to 6 hours. Action potential upstrokes and propagation velocity (theta) were measured with multisite optical recording of transmembrane voltage of the cells stained with the voltage-sensitive dye RH237. Expression of the gap junction protein connexin43 (Cx43) and the fascia adherens junction protein N-cadherin was measured immunohistochemically in the same preparations. Pulsatile stretch caused dramatic upregulation of intercellular junction proteins after only 1 hour and a further increase after 6 hours (Cx43 signal increased from 0.73 to 1.86 and 2.02% cell area, and N-cadherin signal increased from 1.21 to 2.11 and 2.74% cell area after 1 and 6 hours, respectively). This was paralleled by an increase in theta from 27 to 35 cm/s after 1 hour and 37 cm/s after 6 hours. No significant change in the upstroke velocity of the action potential or cell size was observed. Increased theta and protein expression were not reversible after 24 hours of relaxation. Nonpulsatile (static) stretch produced qualitatively similar but significantly smaller changes than pulsatile stretch. Thus, pulsatile linear stretch in vitro causes marked upregulation of proteins that form electrical and mechanical junctions, as well as a concomitant increase in propagation velocity. These changes may contribute to arrhythmogenesis in myocardium exposed to acute stretch.