Abstract

The augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. To determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics, mild lower body negative pressure (LBNP, -30 mmHg) was applied to 29 men. Middle cerebral artery blood flow velocity (MCAv) was measured by transcranial Doppler technique. Stroke volume (SV) was estimated by the Modelflow method with adjustment by the Doppler ultrasound-measured SV at rest. SV, peak and pulsatile MCAv, and pulsatility index were significantly lower during the LBNP stimulation than those at the baseline (e.g., supine resting) (P < 0.05 for all), whereas mean arterial pressure and mean MCAv remained unchanged. The change in SV with the LBNP stimulation significantly correlated with corresponding changes in peak and pulsatile MCAv (r = 0.617, P < 0.001; r = 0.413, P = 0.026, respectively). These results suggest that pulsatile components of cerebrovascular hemodynamics are dampened during the transient period of orthostatic challenge (as simulated using LBNP) when compared to supine rest, and which is partly due to the modified SV.

Highlights

  • There is a gaining recognition that augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease

  • We hypothesized that pulsatile components of cerebrovascular hemodynamics are dampened during the transient period of an orthostatic challenge when compared to supine rest because of the decreased stroke volume (SV)

  • Systolic blood pressures (SBP), mean arterial pressure (MAP), and mean Middle cerebral artery blood flow velocity (MCAv) remained unchanged during the lower body negative pressure (LBNP) stimulation

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Summary

Introduction

There is a gaining recognition that augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. The brain, a high flow organ, is sensitive to excessive pressure and flow pulsatility (Mitchell, 2008). Stroke volume (SV) is greater than that in the upright position because the reduced hydrostatic pressure facilitates the venous return, and which increases cardiac preload (Rowell, 1986). The impact of posture on cerebral hemodynamics, pulsatility, is fully unknown (Bode, 1991). The aim of this study was to determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics.

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