Abstract

IntroductionPrior studies have independently demonstrated that subjects with higher tolerance to simulated hemorrhage elicited by lower body negative pressure (LBNP) exhibit maintenance of cerebral tissue oxygenation, and higher amplitude in spontaneously generated low frequency (~0.1 Hz) oscillations in arterial pressure and cerebral blood flow. We hypothesized that these two independent observations are related, wherein subjects with higher tolerance to LBNP would exhibit increased low frequency power in arterial pressure and cerebral blood flow, which may contribute to the protection of cerebral tissue oxygenation.MethodsHealthy male (n=19, 25±1 y) and female (n=13, 28±1 y) subjects participated in a stepwise LBNP protocol to pre‐syncope. Mean arterial pressure (MAP), middle cerebral artery velocity (MCAv), cerebral tissue oxygen saturation (ScO2), and end tidal CO2 (etCO2) were measured continuously. Subjects were classified as high tolerant if they completed the −60 mmHg step of LBNP. Low frequency oscillations in MAP and MCAv were assessed in the 0.04–0.15 Hz range. Both time and frequency domain data were analyzed using a linear mixed model analysis of variance with Tukey post hoc tests. Comparisons were made at baseline across LBNP stages (−15, −30, −45, and −60 mmHg).ResultsOf the 32 subjects tested, 20 were classified as high tolerant and 12 as low tolerant. No differences were observed between high and low tolerant subjects in MAP (P=0.28), low frequency power of MAP (P=0.13), or low frequency power of MCAv (P=0.24) during LBNP. However, high tolerant subjects exhibited greater protection against reductions in ScO2 (P<0.01), MCAv (P<0.01), and etCO2 (P<0.01) compared to low tolerant subjects during LBNP.ConclusionContrary to our hypothesis, low frequency oscillations in MAP and MCAv did not account for the observed protection in ScO2 for high tolerant subjects. Rather, maintenance of oxygen delivery (indexed via MCAv) appeared to account for the protection in cerebral oxygenation in this cohort of young, healthy subjects.Support or Funding InformationFunding for this study was provided by the U.S. Army MRMC Combat Casualty Care Research Program Grant # W81XWH‐11‐2‐0137, and a contract with Pendar Medical LLC. The content is solely the responsibility of the authors and does not necessarily represent the official views the US Department of Defense.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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