Effect of hematocrit variations on cerebral blood flow and basilar artery diameter in vivo

Background and Purpose-Sickle cell disease (SCD) is associated with cerebral hyperperfusion and an increased risk of stroke. Also, both recurrent microvascular obstruction and chronic hemolysis affect endothelial function, potentially interfering with systemic and cerebral blood flow control. We addressed the question whether cerebrovascular control in patients with SCD is affected and related to hemolysis. Methods-Systemic and cerebrovascular control were studied in 18 patients with SCD and 10 healthy subjects. Dynamic cerebral autoregulation was evaluated by transfer function analysis assessing the relationship between mean cerebral blood flow velocity and mean arterial pressure. Results-Normal baroreflex sensitivity and postural cardiovascular reflex responses indicated integrity of systemic cardiovascular control. In the low-(0.07 to 0.15 Hz) frequency region, mean arterial pressure variability was comparable for both groups, but a larger mean cerebral blood flow velocity variability in SCD (6.

Section: Discussionmentioning

confidence: 96%

Dynamic Cerebral Autoregulation in Homozygous Sickle Cell Disease

Kim

Nur²,

Beers³

et al. 2009

“…Hemodilution does not significantly dilate the basilar artery of cats. 9 In humans the diameter of a large cerebral artery with an internal diameter greater than 2.5 mm does not change significantly during alterations in blood osmolality and Pacc^. 10 We investigated the blood flow velocity from the main trunks of the middle cerebral artery and the basilar artery in our patients.…”

Section: Discussionmentioning

confidence: 99%

Effects of hemodialysis on cerebral circulation evaluated by transcranial Doppler ultrasonography.

Hata

Matsumoto

Handa

et al. 1994

The effects of hemodialysis on the cerebral circulation of humans and the correlation between changes in blood flow velocity in the basal cerebral arteries and those of several physiological variables influenced by hemodialysis have been inadequately studied. Blood flow velocities were obtained from the middle cerebral artery and the basilar artery by transcranial Doppler ultrasonography in 27 patients receiving chronic maintenance hemodialysis immediately before and after the procedure. Changes in body weight, hematocrit, blood pressure, and arterial blood gases were recorded simultaneously. There was a significant reduction in mean flow velocity in the middle cerebral artery (P < .01) and the basilar artery (P < .01) after hemodialysis. We observed a significant negative correlation between the relative change in mean flow velocity and the loss of weight after hemodialysis, the amount of fluid removed, and the increase in hematocrit in the middle cerebral artery and the basilar artery. Hemodialysis and the associated physiological changes can significantly affect the cerebral circulation. Blood flow velocities in the middle cerebral artery and the basilar artery decrease significantly with hemodialysis. The loss of body weight, the amount of fluid removed, and the change in hematocrit significantly correlate with the change in mean flow velocity. The transcranial Doppler method can effectively monitor rapid changes in the cerebral circulation during potentially harmful procedures.

“…Such a vasodilation of large arteries was also speculated by Hudack et al to explain elevation of blood flow secondary to hemodilution 32 despite associated arteriolar constriction. 33 Conversely, Muizelaar et al 34 challenged this hypothesis and proved that hemodilution was in fact accompanied by moderate vasoconstriction of large arteries in vivo, probably acting as a compensatory measure to disproportionate viscosity reduction at the microcirculatory level. They assumed, however, that the vascular bed was not affected by hemodilution and that there was no vascular recruitment.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Consequences of Cerebral Vasospasm on Perforating Arteries

Soustiel

Levy

Bibi

et al. 2001

Background and Purpose-Hemodynamics of cerebral vasospasm after subarachnoid hemorrhage remain unclear, and the discrepancy between ultrasonographic or angiographic evidence of arterial narrowing and neurological ischemic deficit is still debated. Most blood flow studies have been involved with large arteries, and thus, very little is known regarding the hemodynamic behavior of small perforating vessels. Patients with symptomatic vasospasm, however, often present with neurological signs suggesting involvement of deep-sited areas of the brain supplied by perforating arteries. Methods-A pulsatile pump was set to provide an outflow of 350 mL/min through a 10-mm-diameter C-flex tube at a perfusion pressure of 130/80 mm Hg. The perfusion fluid used was prepared to approximate blood viscosity. Perforating arteries were simulated by a 1-mm tube connected to the parent tube at a 90°angle. Cylindrical stenotic devices of decreasing diameters were then introduced into the parent tube at the level of the aperture of the secondary tube and 1.5 diameters upstream of it. Velocity profiles both proximal and distal to the stenosis in the parent tube were obtained with a newly developed ultrasonographic flowmeter that allows for high spatial resolution. Results-Increasing stenosis resulted in decreased outflow in the main tube, although it was significant only with severe stenosis. Whenever the simulated stenosis was placed upstream of the secondary tube, flow reduction was associated with a progressive change in the velocity profile, which gradually changed from laminar conditions to a jet stream limited to the center of the lumen. Further diameter reduction was responsible for the occurrence of flow separation with retrograde flow velocities in the periphery of the lumen. In the secondary tube, flow reduction was much more pronounced and began at a lesser degree of stenosis. Increasing fluid viscosity and decreasing perfusion pressure enhanced flow separation and prominently affected the outflow in the secondary tube. Conversely, whenever the simulated stenosis involved the branching area of the secondary tube, there was a slightly progressive decrease in the relative flow in the main tube as the stenosis became tighter. When the stenosis equaled the diameter of the secondary tube, the relative contribution of the secondary tube increased markedly at the expense of the main tube outflow. Conclusions-The present results show that local cerebral vasospasm induces changes in postvasospastic velocity profile affecting the shear rate and may eventually lead to flow separation. This phenomenon may, in turn, result in a venturi-like effect over the aperture of perforating arteries branching out of the postvasospastic portion of the affected parent artery. These alterations of cerebral hemodynamics may account for at least part of the vasospasm symptomatology, especially in the vertebrobasilar system, where vasospasm is commonly focal rather than diffuse. Furthermore, these changes proved to be affected significantly by manipulations ...