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

Abstract

IntroductionHemorrhage is a leading cause of death from traumatic injury in both the military and civilian populations. Use of lower body negative pressure (LBNP) as a model of hemorrhage in humans has revealed that there is a spectrum of tolerance to this stress. Recent evidence from our laboratory suggests that low frequency (LF; ~0.1 Hz) oscillations in mean arterial pressure (MAP) and middle cerebral artery velocity (MCAv) play a role in this tolerance; high tolerant subjects exhibit greater LF power in MAP and MCAv when compared to low tolerant subjects. We hypothesize that exogenously inducing LF oscillations via oscillatory LBNP (OLBNP) will attenuate reductions in cerebral blood flow and oxygenation during simulated hemorrhagic stress.Methods11 young, healthy subjects (9M/2F) were exposed to two LBNP profiles with an average chamber pressure of −60 mmHg in a randomized and counterbalanced design: 1) static LBNP (0 Hz) and, 2) oscillatory LBNP (0.1 Hz). During both profiles, chamber pressure was gradually reduced to −60 mmHg over 1‐min after which pressure remained at −60 mmHg (0 Hz) for 9‐min or oscillated between −30 mmHg and −90 mmHg (0.1 Hz) for 9‐min. Profiles were separated by a 5‐min recovery. Physiological measurements included arterial pressure and stroke volume via finger photoplethysmography, MCAv via transcranial Doppler ultrasound, and regional 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.ResultsNo 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 the stroke volume response (0 Hz, −42.6±2.5 % vs. 0.1 Hz, −30.6±2.5 %; P<0.001). Importantly, 8/11 subjects completed the 0.1 Hz profile compared with just 5/11 subjects for the 0 Hz profile (P=0.048).DiscussionIn partial support of our hypothesis, cerebral oxygenation was protected during the 0.1 Hz OLBNP profile. While MCAv was similar between conditions, we propose that the oscillatory pattern of cerebral blood flow may elicit a shear‐stress induced vasodilation, so assessment of velocity may be masking an increase in flow. This possibility is further supported by the finding that stroke volume was also protected during the 0.1 Hz profile, which may reflect an increase in venous return during the upstroke period of the OLBNP profile. 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 a hemorrhagic stress.Support or Funding InformationUNTHSC ICMD Junior Faculty Seed GrantThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.