Peak Analysis of Cerebral Blood Velocity Responses to Forced Low Frequency Oscillations during Simulated Hemorrhagic Stress in Humans

Abstract

Peak Analysis of Cerebral Blood Velocity Responses to Forced Low Frequency Oscillations during Simulated Hemorrhagic Stress in Humans Haley J. Barnes, B.S., Garen K. Anderson, M.S., Alexander J. Rosenberg, Ph.D., Flora S. Park, M.S., Justin D. Sprick, Ph.D., Caroline A. Rickards, Ph.D Purpose: Tolerance to blood loss injuries (actual and simulated) varies across individuals. Higher amplitude of low frequency oscillations (10-s cycle; ~0.1 Hz) in brain blood flow and arterial pressure have been associated with higher tolerance to simulated hypovolemic episodes using lower body negative pressure (LBNP). We have previously demonstrated that forcing oscillations in cerebral blood flow and arterial pressure at 0.1 Hz and 0.05 Hz with oscillatory LBNP (OLBNP) protects cerebral oxygenation during central hypovolemia. However, there was no protection of mean cerebral blood flow (indexed via mean middle cerebral artery velocity, MCAv) with these oscillatory conditions. We hypothesize that the peak mean MCAv will be higher in the 0.05 Hz and 0.1 Hz OLBNP conditions compared to the 0 Hz condition, which may account for the protection of cerebral tissue oxygenation. Methods: Fourteen healthy human subjects (3 female/11 male) were randomly exposed to 10-min of non-oscillatory (0 Hz) and oscillatory (0.05 Hz and 0.1 Hz) LBNP conditions with an average LBNP chamber pressure of -60 mmHg. Measurements included MCAv via transcranial Doppler ultrasound, frontal lobe cerebral oxygenation (ScO2) via near infrared spectroscopy, and stroke volume and arterial pressure via finger photoplethysmography. Peak analysis was performed in 10-s and 5-s windows for the 0.05 Hz and 0.1 Hz profiles, respectively. Peak responses to the three LBNP conditions were compared using a linear mixed model for repeated measures with Tukey post hoc tests. Results: As previously reported, tolerance to the two OLBNP conditions was higher compared to the 0 Hz condition (P ≤ 0.09 for both vs. 0 Hz). In partial support of our hypothesis, when compared to the 0 Hz profile, the peak MCAv was higher with 0.05 Hz OLBNP (51.0±4.2 cm/s vs. 46.3±3.4 cm/s; P = 0.004) but not with the 0.1 Hz profile (49.0±3.9 cm/s; P = 0.11 vs. 0 Hz). Conclusions: The higher peak MCAv during the 0.05 Hz OLBNP profile may contribute to the attenuated decrease in cerebral oxygenation. These findings demonstrate the potential contribution of oscillatory peaks in cerebral blood flow to the protection of cerebral oxygenation and increased tolerance to simulated hemorrhage.