Baroreflex-induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans

Abstract

We investigated the effect of baroreflex-induced sympathetic activation, produced by lower body negative pressure (LBNP) at -40 mmHg, on cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end-tidal carbon dioxide pressure (PET,CO2) of +10, +5, 0, -5, and -10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO2 and CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 +/- 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady-state hypercapnia (3.14 +/- 0.24 vs. 2.96 +/- 0.26 cm s-1 mmHg-1) or hypocapnia (1.31 +/- 0.18 vs. 1.32 +/- 0.19 cm s-1 mmHg-1), or the CFV responses to voluntary apnoea (+51 +/- 19 vs. +50 +/- 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex-induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.

Figure 2. Relationships between P_ET,CO2 and CFV and mean arterial pressure (MAP) with (•) and without (○) LBNP

Data shown are means ± s.e.m., n = 10.

Figure 1. Individual cerebral flow velocity responses to hyper- and hypocapnia with (•) and without (○) lower body negative pressure (LBNP)

Continuous and dashed lines represent linear regressions of velocity on P_ET,CO2, calculated separately for hyper- and hypocapnia.

Figure 3. Cerebrovascular responses to 20 s breath holds with (•) and without (○) LBNP

The dashed vertical lines indicate the duration of the apnoea. Data shown are means ± s.e.m., n = 6.