Mechanism and pattern of human cerebrovascular regulation after rapid changes in blood CO2 tension.

Abstract

The relationships between cerebral blood flow and blood CO2 tension [PCO2] after rapid alterations in inspired CO2 were explored in 37 senarate studies on 13 normal male volunteers. During progressive stepwise increases and decreases in arterial PCO2 above the control level, jugular venous PCO2 correlated more exactly with cerebral blood flow than did the arterial PCO2 In 16 of 19 experiments arterial PCO2 described a counterclockwise loop when plotted against the corresponding values for cerebral blood flow. This distinct hysteresis between arterial PCO2 and cerebral blood flow was evident in only 1 of 10 experiments during stepwise reductions and return to control in the hypocapnic range, which was accomplished by variable levels of hyperventilation. On 10 occasions cerebral blood flow and arterial PCO2 were measured as rapidly as possible after a single breath of 28. 5% CO2. These studies provided further evidence that a finite interval is required for the cerebral vessels to respond to a given elevation in arterial PCO2. The data are interpreted to suggest that the tissue tension of CO2 may be the effective regulatory of cerebrovascular resistance rather than the intra-arterial tension of this gas. Thus, measurements restricted to arterial PCO2 during ascent of arterial PCO2 may overestimate and, during descent of this tension, underestimate the actual determinant of cerebrovascular resistance when these measurements are made in the rapidly or continuously changing state.