Interaction of carbon dioxide and sympathetic nervous system activity in the regulation of cerebral perfusion in humans

Recent studies suggest that activation of the sympathetic nervous system either directly or indirectly influences cerebrovascular tone in humans even within the autoregulatory range. In 6 healthy subjects (aged 29+/-4 years), we used transcranial Doppler sonography to determine cerebral blood flow velocity during sympathetic activation elicited through head-up tilt (HUT) and sympathetic deactivation through ganglionic blockade. PaCO2 was manipulated through hyperventilation and CO2 breathing (5%). With subjects in the supine position and during HUT, mean arterial pressure was not influenced by PaCO2. During ganglionic blockade, mean arterial pressure decreased markedly with hyperventilation (-13+/-1.9 mm Hg). Manipulation of sympathetic tone elicited only mild changes in cerebral blood flow (64+/-5.8 cm/s supine, 58+/-4.9 cm/s upright, and 66+/-6.2 cm/s during ganglionic blockade; P=0.07 by ANOVA). The slope of the regression between PaCO2 and mean velocity was 1.6+/-0.18 cm/(s . mmHg) supine, 1.3+/-0.14 cm/(s . mm Hg) during HUT, and 2.3 +/- 0.36 cm/(s . mm Hg) during ganglionic blockade (P<0.05). Spontaneous PaCO2 and ventilatory response to hypercapnia were also modulated by the level of sympathetic activity, Changes in sympathetic tone have a limited effect on cerebral blood flow at normal PaCO2 levels. However, the sympathetic nervous system seems to attenuate the CO2-induced increase in cerebral blood flow. This phenomenon may indicate a moderate direct effect of the sympathetic nervous system on the cerebral vasculature. Furthermore, sympathetic activation tends to increase ventilation and thus can indirectly increase cerebrovascular tone.