Hemorrhage at high altitude: impact of sustained hypobaric hypoxia on cerebral blood flow, tissue oxygenation, and tolerance to simulated hemorrhage in humans - PubMed (original) (raw)

Hemorrhage at high altitude: impact of sustained hypobaric hypoxia on cerebral blood flow, tissue oxygenation, and tolerance to simulated hemorrhage in humans

Alexander J Rosenberg et al. Eur J Appl Physiol. 2024 Aug.

Abstract

With ascent to high altitude (HA), compensatory increases in cerebral blood flow and oxygen delivery must occur to preserve cerebral metabolism and consciousness. We hypothesized that this compensation in cerebral blood flow and oxygen delivery preserves tolerance to simulated hemorrhage (via lower body negative pressure, LBNP), such that tolerance is similar during sustained exposure to HA vs. low altitude (LA). Healthy humans (4F/4 M) participated in LBNP protocols to presyncope at LA (1130 m) and 5-7 days following ascent to HA (3800 m). Internal carotid artery (ICA) blood flow, cerebral delivery of oxygen (CDO2) through the ICA, and cerebral tissue oxygen saturation (ScO2) were determined. LBNP tolerance was similar between conditions (LA: 1276 ± 304 s vs. HA: 1208 ± 306 s; P = 0.58). Overall, ICA blood flow and CDO2 were elevated at HA vs. LA (P ≤ 0.01) and decreased with LBNP under both conditions (P < 0.0001), but there was no effect of altitude on ScO2 responses (P = 0.59). Thus, sustained exposure to hypobaric hypoxia did not negatively impact tolerance to simulated hemorrhage. These data demonstrate the robustness of compensatory physiological mechanisms that preserve human cerebral blood flow and oxygen delivery during sustained hypoxia, ensuring cerebral tissue metabolism and neuronal function is maintained.

Keywords: Central hypovolemia; Cerebral blood velocity; Hypoxia; Internal carotid artery blood flow; Lower body negative pressure.

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Conflict of interest statement

Conflict of interest None of the authors have any conflicts of interest.

Figures

Fig. 1

Lower body negative pressure (LBNP) protocol (Panel A), consisting of a 5-min baseline period, then application of LBNP to – 60 mmHg for 10-min, followed by decreases in chamber pressure every 5-min to – 70, – 80, – 90 and – 100 mmHg, until pre-syncope. Tolerance time (in seconds; Panel B) to lower body negative pressure (LBNP) at low altitude (LA) and at high altitude (HA) in 8 participants. Stroke volume (SV; Panel C) was higher at HA (dashed line, open circles) compared with LA (solid line, closed circles), but decreased by a similar magnitude at both altitudes (Panel D). Mean ± SD and/or individual participant data (circles) are presented. *Denotes difference from baseline, P ≤ 0.001. †Denotes difference between LA and HA, P ≤ 0.06. A two-factor (time, altitude) linear mixed model analysis with Holm-corrected post hoc tests run on the least squared means (data in Panel C), and paired _t_-tests (data in Panels B and D) were used for analysis

Fig. 2

Internal carotid artery (ICA) blood flow (Panel A) decreased at low altitude (solid line, closed circle) and high altitude (dashed line, open circle) during lower body negative pressure (LBNP) to presyncope (PS-1). While ICA blood flow was higher at HA baseline, the magnitude of change was similar with LBNP at both altitudes (Panel B). Cerebral delivery of oxygen (Panel C) was higher at high altitude (dashed line, open circle) vs. low altitude (solid line, closed circle) at baseline and at pre-syncope (PS-1) but decreased by the same magnitude at both altitudes (Panel D). Mean ± SD and/or individual participant data (circles) are presented. *Denotes difference from baseline, P ≤ 0.003. †Denotes difference between low and high altitude, P ≤ 0.09. A two-factor (time, altitude) linear mixed model analysis with Holm-corrected post hoc tests run on the least squared means (data in Panels A and C), and paired _t_-tests (data in Panels B and D) were used for analysis

Fig. 3

Cerebral oxygen saturation (Panel A) decreased at low altitude (solid line, closed circle) and high altitude (solid line, open circle) during lower body negative pressure (LBNP), but there was no difference between altitude conditions in either absolute or relative responses (Panel B). Mean ± SD and/or individual participant data (circles) are presented. A two-factor (time, altitude) linear mixed model analysis with Holm-corrected post hoc tests run on the least squared means (data in Panel A), and paired _t_-tests (data in Panel B) were used for analysis

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Hemorrhage at high altitude: impact of sustained hypobaric hypoxia on cerebral blood flow, tissue oxygenation, and tolerance to simulated hemorrhage in humans - PubMed (original) (raw)