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Received May 11, 2003
Accepted after revision June 9, 2003
1 Departments of Medicine and Orthopedics, University of Wisconsin-Madison and the Middleton Veterans Administration Hospital, Madison, Wisconsin 53705, USA
2 Departments of Medicine and Orthopedics and Rehabilitation, University of Wisconsin-Madison and the Middleton Veterans Administration Hospital, Madison, Wisconsin 53705, USA
3 Department of Orthopedics and Rehabilitation, 1300 University Avenue, 5173 MSC, Madison, WI 53706-1532, USA
* To whom correspondence should be addressed. E-mail: morgan{at}surgery.wisc.edu.
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.
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