Responses to Pulsatile Flow in Piglet Isolated Cerebral Arteries

Abstract

Because cerebrovascular hemorrhage in newborns is often associated with fluctuations in cerebral blood flow, this study was designed to investigate the effects of pulsatile flow in isolated cerebral arteries from neonatal piglets. Arteries mounted on cannulas were bathed in and perfused with a physiologic saline solution. An electronic system produced pulsations, the amplitude and frequency of which were independently controlled. At constant mean transmural pressure (20 mm Hg), increasing flow in steps from 0 to 1.6 mL/min under steady flow conditions caused a biphasic response, constriction at low flow, and dilation at high flow. Under pulsatile flow conditions (pulse amplitude 16-24 mm Hg; 2 Hz), the arteries dilated upon flow initiation and continued to dilate as mean flow increased. Dilation to pulsatile flow did not depend on the level of mean flow because switching from steady to pulsatile flow at each flow step also caused dilation. Arteries dilated further upon increasing either pulse amplitude (12-28 mm Hg; 2 Hz) or frequency (16-24 mm Hg; 4 Hz). Inhibiting nitric oxide synthesis with Nomega-nitro-L-arginine or perfusing with glutaraldehyde to decrease endothelial cell deformability significantly reduced dilations to pulsatile flow and to increased amplitude and frequency. These data suggest that the arterial response to flow is highly dependent on the mode of flow. Dilation induced by initiating pulsatile flow or increasing either pulse amplitude or frequency appears to be mediated by augmented nitric oxide release as result of shear stress-induced deformation of the endothelial cells.

Heat Shock Protein 90 Is Involved in Pulsatile Flow-Induced Dilation of Rat Middle Cerebral Artery

“…Using an isolated artery system similar to that of ours, Shimoda et al [3]recently demonstrated that piglet cerebral arteries dilate in response to pulsatile flow. Our findings show that cerebral arteries from adult rats also dilate in response to pulsatile flow, and that activation of eNOS is responsible for the observed dilation.…”

“…Since active vascular resistance in vivo is determined primarily by the tone of small arteries [2], it is important to study cellular responses of cells in the wall of such arteries to hemodynamic factors. Pulsatile flow in isolated cerebral arteries from piglets has been found to induce dilation which was dependent on the activity of nitric oxide synthase (NOS) [3]. However, whether dilation of the artery by pulsatile flow is unique to neonatal cerebral arteries and the mechanism by which an acute change in pulsatility causes activation of NOS is not clear.…”

Is the vascular endothelium under the control of aldosterone? Facts and hypothesis

“…As aldosterone increases the stiffness of a contracted endothelial cell and elevates its intracellular pressure, it is probable that it is the increased stiffness of the cell that reduces NO release. This assumption is based upon the evidence that a pulsating flow of blood exerts shear forces at the endothelial cell wall and the supposition that when such a cell becomes stiffer it will be more difficult to deform and thus reduce its synthesis and release of NO [39].…”

Neuroprotective Effect of <i>L</i>-Arginine in a Newborn Rat Model of Acute Severe Asphyxia

“…Accordingly, a signifi cant increase of eNOS expression has been observed in the ischemic brain in the fi rst 24 h after a hypoxic-ischemic insult in newborn rats [14] . Inhibition of eNOS abolishes the in vitro autoregulatory response of cerebral arteries to changes in intraluminal pressure [15] or fl ow [16] .…”