Background and Purpose-The relationship between middle cerebral artery (MCA) flow velocity (CFV) and cerebral blood flow (CBF) is uncertain because of unknown vessel diameter response to physiological stimuli. The purpose of this study was to directly examine the effect of a simulated orthostatic stress (lower body negative pressure [LBNP]) as well as increased or decreased end-tidal carbon dioxide partial pressure (P ET CO 2 ) on MCA diameter and CFV. Methods-Twelve subjects participated in a CO 2 manipulation protocol and/or an LBNP protocol. In the CO 2 manipulation protocol, subjects breathed room air (normocapnia) or 6% inspired CO 2 (hypercapnia), or they hyperventilated to Ϸ25 mm Hg P ET CO 2 (hypocapnia). In the LBNP protocol, subjects experienced 10 minutes each of Ϫ20 and Ϫ40 mm Hg lower body suction. CFV and diameter of the MCA were measured by transcranial Doppler and MRI, respectively, during the experimental protocols. Results-Compared with normocapnia, hypercapnia produced increases in both P ET CO 2 (from 36Ϯ3 to 40Ϯ4 mm Hg, PϽ0.05) and CFV (from 63Ϯ4 to 80Ϯ6 cm/s, PϽ0.001) but did not change MCA diameters (from 2.9Ϯ0.3 to 2.8Ϯ0.3 mm). Hypocapnia produced decreases in both P ET CO 2 (24Ϯ2 mm Hg, PϽ0.005) and CFV (43Ϯ7 cm/s, PϽ0.001) compared with normocapnia, with no change in MCA diameters (from 2.9Ϯ0.3 to 2.9Ϯ0.4 mm). During Ϫ40 mm Hg LBNP, P ET CO 2 was not changed, but CFV (55Ϯ4 cm/s) was reduced from baseline (58Ϯ4 cm/s, PϽ0.05), with no change in MCA diameter. Conclusions-Under the conditions of this study, changes in MCA diameter were not detected. Therefore, we conclude that relative changes in CFV were representative of changes in CBF during the physiological stimuli of moderate LBNP or changes in P ET CO 2 .

To establish the accuracy of transcranial Doppler ultrasound (TCD) measures of middle cerebral artery (MCA) cerebral blood flow velocity (CBFV) as a surrogate of cerebral blood flow (CBF) during hypercapnia (HC) and hypocapnia (HO), we examined whether the cross-sectional area (CSA) of the MCA changed during HC or HO and whether TCD-based estimates of CBFV were equivalent to estimates from phase contrast (PC) magnetic resonance imaging. MCA CSA was measured from 3T magnetic resonance images during baseline, HO (hyperventilation at 30 breaths/min), and HC (6% carbon dioxide). PC and TCD measures of CBFV were measured during these protocols on separate days. CSA and TCD CBFV were used to calculate CBF. During HC, CSA increased from 5.6 ± 0.8 to 6.5 ± 1.0 mm(2) (P < 0.001, n = 13), while end-tidal carbon dioxide partial pressure (PETCO2) increased from 37 ± 3 to 46 ± 5 Torr (P < 0.001). During HO, CSA decreased from 5.8 ± 0.9 to 5.3 ± 0.9 mm(2) (P < 0.001, n = 15), while PetCO2 decreased from 36 ± 4 to 23 ± 3 Torr (P < 0.001). CBFVs during baseline, HO, and HC were compared between PC and TCD, and the intraclass correlation coefficient was 0.83 (P < 0.001). The relative increase from baseline was 18 ± 8% greater (P < 0.001) for CBF than TCD CBFV during HC, and the relative decrease of CBF during HO was 7 ± 4% greater than the change in TCD CBFV (P < 0.001). These findings challenge the assumption that the CSA of the MCA does not change over modest changes in PETCO2.

No abstract

No abstract

The purpose of the present study was to determine the cortical structures involved with integrated baroreceptor-mediated modulation of autonomic cardiovascular function in conscious humans independent of changes in arterial blood pressure. We assessed the brain regions associated with lower body negative pressure (LBNP)-induced baroreflex control using functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast in eight healthy male volunteer subjects. The levels of LBNP administered were 5, 15 and 35 mmHg. Heart rate (HR; representing the cardiovascular response) and LBNP (representing the baroreceptor activation level) were simultaneously monitored during the scanning period. In addition, estimated central venous pressure (CVP), arterial blood pressure (ABP) and muscle sympathetic nerve activity were recorded on a separate session. Random effects analyses (SPM2) were used to evaluate significant (P < 0.05) BOLD signal changes that correlated separately with both LBNP and HR (15-and 35-mmHg versus 5-mmHg LBNP). Compared to baseline, steady-state LBNP at 15 and 35 mmHg decreased CVP (from 7 ± 1 to 5 ± 1 and 4 ± 1 mmHg, respectively) and increased MSNA (from 12 ± 1 to 23 ± 3 and 36 ± 4 bursts min −1 , respectively, both P < 0.05 versus baseline). Furthermore, steady-state LBNP elevated HR from 54 ± 2 beats min −1 at baseline to 64 ± 2 beats min −1 at 35-mmHg suction. Both mean arterial and pulse pressure were not different between rest and any level of LBNP. Cortical regions demonstrating increased activity that correlated with higher HR and greater LBNP included the right superior posterior insula, frontoparietal cortex and the left cerebellum. Conversely, using the identical statistical paradigm, bilateral anterior insular cortices, the right anterior cingulate, orbitofrontal cortex, amygdala, midbrain and mediodorsal nucleus of the thalamus showed decreased neural activation. These data corroborate previous investigations highlighting the involved roles of the insula, anterior cingulate cortex and amygdala in central autonomic cardiovascular control. In addition, we have provided the first evidence for the identification of the cortical network involved specifically with baroreflex-mediated autonomic cardiovascular function in conscious humans.