Phenylephrine decreases frontal lobe oxygenation at rest but not during moderately intense exercise

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Abstract
Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity (Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2, and arterial Pco2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. In randomized order, a bolus of saline or 0.3 mg of phenylephrine was then injected during semisupine cycling, eliciting a low (∼110 beats/min) or a high (∼150 beats/min) heart rate. At rest, MAP and MCA Vmean increased ∼20% (P < 0.001) and ∼10% (P < 0.001 for 0.25 mg of phenylephrine and P < 0.05 for 0.4 mg of phenylephrine), respectively. ScO2 then decreased ∼7% (P < 0.001). Phenylephrine had no effect on SjvO2, PaCO2, or CMRO2. MAP increased after the administration of phenylephrine during low-intensity exercise (∼15%), but this was attenuated (∼10%) during high-intensity exercise (P < 0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (−5%, P < 0.001) and abolished during high-intensity exercise (−3%, P = not significant), where PaCO2 decreased 7% (P < 0.05) and CMRO2 increased 17% (P < 0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.