Responses of cerebral blood flow and tissue oxygenation to low frequency oscillations during simulated hemorrhagic stress in humans

Introduction: Tolerance to both actual and simulated hemorrhage varies between individuals. Low frequency (LF; ~0.1 Hz) oscillations in mean arterial pressure (MAP) and brain blood flow (indexed via middle cerebral artery velocity, MCAv), may play a role in tolerance to reduced central blood volume; subjects with high tolerance to simulated hemorrhage induced via application of lower body negative pressure (LBNP) exhibit greater LF power in MAP and MCAv compared to low tolerant subjects. The mechanism for this association has not been explored. We hypothesized that inducing LF oscillations would attenuate reductions in cerebral blood flow and oxygenation during simulated hemorrhage. Methods: 11 subjects (9M/2F) were exposed to two LBNP profiles with an average chamber pressure of -60 mmHg: 1) 0 Hz - chamber pressure remained at -60 mmHg for 9-min, or 2) 0.1 Hz - chamber pressure oscillated between -30 mmHg and -90 mmHg at a frequency of 0.1 Hz for 9-min. Profiles were separated by a 5-min recovery. Measurements included arterial pressure and stroke volume via finger photoplethysmography, MCAv via transcranial Doppler ultrasound, and cerebral oxygenation of the frontal lobe (ScO2) via near infrared spectroscopy. Hemodynamic data was analyzed using a paired t-test. Tolerance was assessed with a Fischer’s exact test. Results: No differences were observed between profiles for MAP (0 Hz, 79.8±2.5 mmHg vs. 0.1 Hz, 80.0±1.9 mmHg; P=0.93) and MCAv (0 Hz, 42.4±3.3 cm/s vs. 0.1 Hz, 43.5±3.7 cm/s P=0.43). The reduction in ScO2 was attenuated (P=0.05) during the 0.1 Hz profile (-4.1±1.2 %) compared to the 0 Hz profile (-6.1±1.1 %). A similar attenuation was observed in stroke volume (0 Hz, -42.6±2.5 % vs. 0.1 Hz, -30.6±2.5 %; P Discussion:In partial support of our hypothesis, cerebral oxygenation was protected during the 0.1 Hz OLBNP profile. While MCAv was similar between conditions, the oscillatory pattern of cerebral blood flow may elicit a shear-stress induced vasodilation, so assessment of velocity may mask an increase in flow. Importantly, more subjects were able to tolerate the 0.1 Hz profile compared to the static 0 Hz profile, despite similar arterial pressure responses. These findings emphasize the potential importance of hemodynamic oscillations in maintaining perfusion and oxygenation of cerebral tissue during hemorrhagic stress.