Cerebral Hemodynamic Response to Hypercapnia Is Diminished During Central Hypovolemia

Abstract

PURPOSE: To examine the regulatory function of cerebral perfusion during central hypovolemia. METHODS: Eight healthy volunteers (25.0±1.1 yr age & 72.0±5.8 kg wt) participated in the study that was approved by IRB at UNT Health Science Center. Central hypovolemia was elicited by lower body negative pressure (LBNP) -15 Torr. Cerebral blood flow velocity of middle cerebral artery (VMCA) and cerebral regional O2 saturation (ScO2) were continuously measured during rebreathing (∼6 min) induced progressive increases in partial pressure of trans-cutaneous CO2 (PTCCO2) at rest (or control) and during LBNP. Continuous cerebral vascular conductance (CVC, the ratio of VMCA to mean arterial pressure) and ScO2 data were averaged every 30 sec and the rate of their percent changes (D) during increases in PTCCO2 was compared. RESULTS: The rebreathing protocol similarly raised PTCCO2 during the control (from 40.0±1.0 to 48.7±1.5 mmHg, P < 0.05) and LBNP (from 38.5±1.2 to 48.6±1.7 mmHg, P < 0.05). This hypercapnia significantly increased both CVC and ScO2. During the control and LBNP conditions, respectively, the slopes of DCVC/PTCCO2 were 4.43±0.36 (R2 =0.93) vs 3.27±0.27 (R2 = 0.92) %/mmHg and the slopes of DScO2/PTCCO2 were 1.56±0.08 (R2 =0.97) vs 1.10±0.08 (R2 =0.94) %/mmHg. They all had significant decrease during LBNP (P < 0.05) as compared with the control. However, the slopes of DScO2/DCVC during hypercapnia were statistically identical, i.e., the control vs LBNP: 0.34±0.02 vs 0.33±0.02. CONCLUSIONS: Central hypovolemia diminished the rate of cerebral vasodilation and oxygenation in response to hypercapnia.