Search

Pulsatile components of blood pressure may arise from forward (ventricular generated) or backward wave travel in the arterial tree. The objective of this study was to determine the relative contributions of forward and backward waves to pulsatility. We used wave intensity and wave separation analysis to determine pulsatile components of blood pressure during inotropic and vasopressor stimulation by dobutamine and norepinephrine in normotensive subjects and compared pulse pressure components in hypertensive (mean+SD, 48.8± 11.3 years; 165±26.6/99+14.2 mmHg) and normotensive subjects (52.2±12.6 years; 120±14.2/71±8.2 mmHg). Dobutamine (7.5 µg/kg per minute) increased the forward compression wave generated by the ventricle and increased pulse pressure from 36.8±3.7 to 59.0+3.4 mmHg (mean±SE) but had no significant effect on mean arterial pressure or the midsystolic backward compression wave. By contrast, norepinephrine (50 ng/kg per minute) had no significant effect on the forward compression wave but increased the midsystolic backward compression wave. Despite this increase in the backward compression wave, and an increase in mean arterial pressure, norepinephrine increased central pulse pressure less than dobutamine (increases of 2 2 .1±3.8 and 7.2±2.8 mmHg for dobutamine and norepinephrine, respectively; P<0.02). An elevated forward wave component (mean±SE, 50.4±3.4 versus 35.2±1.8 mmHg, in hypertensive and normotensive subjects, respectively; P<0.001) accounted for approximately two thirds of the total difference in central pulse pressures between hypertensive and normotensive subjects. Increased central pulse pressure during inotropic stimulation and in essential hypertension results primarily from the forward compression wave. [ABSTRACT FROM AUTHOR]

The article examines the relative specificity of vasodilator drugs for radial artery and forearm resistance vessels during intrabrachial arterial infusion. The nitric oxide (NO) donors, were compared with the a-adrenergic antagonist phentolamine, calcium-channel antagonist verapamil and hyrdralazine. The differential response to NO donors suggests that there is potential to manipulate the downstream pathway to confer greater specificity for large arteries.

Flow-mediated dilation of the brachial or radial artery in response to transient hyperaemic flow, the most widely used test of endothelial function, is only manifest after flow decays back to baseline. We examined whether this dissociation of flow and diameter might be explained by a reduction in transmural pressure generated by high flow. Studies were performed in healthy subjects 20 to 55 years of age. Flow-mediated dilation was measured in the radial artery using a standard protocol and after flow interruption at peak hyperemia during brachial artery infusion of saline and the NO synthase inhibitor N(G)-monomethyl-L-arginine (8 μmol/min). Flow interruption 20 seconds after cuff release (during high flow but no dilatation) produced an immediate increase in radial artery diameter of 5.36±2.12%, inhibited by N(G)-monomethyl-L-arginine to 1.09±0.67% (n=8; P<0.001). Mean intra-arterial radial blood pressure and, hence, transmural pressure fell after cuff release by a mean of 26±1.8 mm Hg (n=6; P<0.0001) at the time of peak hyperemic flow. Modulation of transmural pressure within the brachial artery by cuff inflation around the artery demonstrated that this fall is sufficient to reduce arterial diameter by an amount similar to flow-mediated dilation. These results suggest that flow-dependent, NO-dependent dilation is offset by a flow-induced fall in local arterial pressure and, hence, in transmural pressure. Shear related NO release is likely to play a greater role in the short-term regulation of arterial tone than that suggested by flow-mediated dilation. [ABSTRACT FROM AUTHOR]