Authors: Querido JS, Ainslie PN, Foster GE, Henderson WR, Halliwill JR, Ayas NT, Sheel AW.
Previous research has shown an inconsistent effect of hypoxia on dynamic cerebral autoregulation (dCA), which may be explained by concurrent CO2 control. To test the hypothesis that hypoxic dCA is mediated by CO2, we assessed dCA (transcranial Doppler) during and following acute normobaric isocapnic and poikilocapnic hypoxic exposures. On two separate days, the squat-stand maneuver was used to determine dCA in healthy subjects (n = 8; 3 female) in isocapnic and poikilocapnic hypoxia exposures (end-tidal oxygen pressure 50 mmHg for 20 min). In isocapnic hypoxia, the amplitude of the cerebral blood flow response to increases and decreases in mean arterial blood pressure (MAP) were elevated (i.e. increases in gain of +35% and +28%, respectively; P < 0.05). However, dCA gain to increases in pressure was reduced compared to baseline (-32%, P < 0.05) following the isocapnic hypoxia exposure. Similarly, intravenous bolus injections of sodium nitroprusside and phenylephrine in a separate group of subjects (n = 8; 4 female) also demonstrated a reduction in dCA gain to hypertension following isocapnic hypoxia. In contrast, dCA gain with the squat-stand maneuver did not significantly change from baseline during or following poikilocapnic hypoxia (P > 0.05). Our results demonstrate that dCA impairment in isocapnic hypoxia can be prevented with hypocapnia, and highlight the integrated nature of hypoxic cerebrovascular control which is under strong CO2 influence.
Full text and source: Journal of applied physiology
J Appl Physiol. 2013 Mar 7.