(603.18) Effects of Sustained Hypobaric Hypoxia on Amplitude of Forced Hemodynamic Oscillations During Central Hypovolemia

Poster Board Number: E464

Garen Anderson (University of North Texas Health Science Center), Alexander Rosenberg (Midwestern University), Haley Barnes (University of North Texas Health Science Center), Jordan Bird (Mount Royal University), Brandon Pentz (Mount Royal University), Britta Byman (Mount Royal University), Nicholas Jendzjowsky (University of Calgary, University of Calgary), Richard Wilson (University of Calgary), Trevor Day (Mount Royal University), Caroline Rickards (University of North Texas Health Science Center)

Introduction: Forcing oscillations in arterial pressure and cerebral blood flow at 0.1 Hz during simulated hemorrhage protects cerebral oxygenation at both low and high altitude. Arterial pressure oscillations at 0.1 Hz are endogenously driven by rhythmic fluctuations in sympathetic nerve activity. As hypobaric hypoxia increases basal sympathetic activity, we hypothesize that the amplitude of forced oscillations in arterial pressure and cerebral blood flow during simulated hemorrhage will be greater at high altitude compared to low altitude.

Methods: 8 healthy human participants (4 M, 24.7 ± 4.1 y; 4 F, 34.3 ± 8.3 y) underwent a hypovolemic oscillatory lower body negative pressure (OLBNP) protocol, where chamber pressure reduced to -60 mmHg then oscillated every 5-s between -30 mmHg and -90 mmHg over 10-min (0.1 Hz). This protocol was performed at both low altitude (LA; Calgary, Alberta, Canada; 1045 m) and high altitude (HA; White Mountain, California, USA; 3800 m). Mean arterial pressure (MAP), mean middle cerebral artery velocity (MCAv), and cerebral tissue oxygenation (ScO2) were recorded continuously. Frequency analysis (via continuous wavelet transform) was used to quantify oscillations in MAP and mean MCAv at ~0.1 Hz. Data were analyzed with linear mixed-models and paired t-tests. All data are represented as mean ± SD.

Results: Baseline amplitude of oscillations were similar between HA and LA for MAP (1.9 ± 0.6 mmHg vs. 1.2 ± 0.5 mmHg; P = 0.47) and mean MCAv (0.9 ± 0.4 cm/s vs. 1.1 ± 0.3 cm/s; P = 0.91). Oscillatory amplitudes increased with 0.1 Hz OLBNP and altitude for MAP (ANOVA main effect, OLBNP: P lt; 0.001, Altitude: P = 0.007) and mean MCAv (ANOVA main effect, OLBNP: P = 0.002, Altitude: P = 0.008). Amplitude of oscillations during OLBNP were greater at HA for both MAP (4.0 ± 2.1 mmHg vs. 2.6 ± 1.4 mmHg, P = 0.05) and mean MCAv (2.4 ± 1.1 cm/s vs. 0.9 ± 0.4 cm/s; P = 0.01). The relative (%∆) decrease in ScO2 was not different between HA and LA (-0.63 ± 0.92 % vs. -2.56 ± 2.61 %, P = 0.11).

Conclusions: Oscillatory amplitudes at 0.1 Hz in both MAP and mean MCAv increased during OLBNP at high altitude. This effect may be due, in part, to the sympathoexcitatory stimulus of hypobaric hypoxia, and does not alter the protection of cerebral tissue oxygenation in this environment.

CAR supported by AHA 17GRNT33671110. TAD supported by RGPIN-2016-04915. RJAW supported by NSERC Discovery Grant. GKA supported by NIH T32AG020494 and AHA 20PRE35210249. AJR supported by NIH 1F32HL144082-01A1. NGJ is a Parker B Francis Fellowship Recipient.