The Baroreflex And Neurogenic Control Of Cerebral Autoregulation In Cerebral Blood Flow
Introduction The neurogenic component of cerebral autoregulation (CA) refers to those mechanisms controlling cerebral blood flow under the influence of the nervous system, and which rely on the innervation of the cerebral blood vessels. The neurogenic control of CA is incompletely understood. Reports of a functional relationship between CA and the baroreflex (BR) have prompted suggestions that the baroreceptors might supply neurogenic input to the cerebral vasculature. Alternative potential inputs have also not been explored. A head up tilt (HUT) protocol offers an established way to investigate CA further. Near-infrared spectroscopy (NIRS) measurements during HUT provide an approach to characterising changes in the cerebral vasculature during orthostatic challenge. Inferences from HUT require knowledge of whether a hydrostatic correction must be applied to blood pressure (BP) measurements taken at heart level to convert them to BP at brain level. Whether such a correction is necessary is not fully understood. Methods Human subjects underwent HUT. Changes in heart rate, BP, cerebral blood flow and NIRS parameters were characterised. These variables were used to assess the appropriateness of hydrostatic correction. The measures were also used to calculate baroreceptor sensitivity (BRS) and CA index which were then compared using correlation techniques and Granger causality analysis. In the second set of experiments, subjects underwent a virtual reality simulation of HUT (VHUT) without gravitational change. Physiological variables were measured as before and responses during HUT and VHUT were compared. Results BP measured at heart level increased during HUT. Hydrostatic correction for BP at the level of the brain resulted in lower values. NIRS revealed an increase in cerebral blood volume which may occur predominantly within the venous compartment. There was no evidence to support a relationship between BRS and CA index. VHUT may result in some change within the cerebral vasculature, but further studies are required. Conclusions The observed cerebral vasodilation is not consistent with the increase in BP found when no hydrostatic correction is applied for determining BP at the level of the brain. Therefore hydrostatic correction is appropriate in HUT studies. The evidence for potential venodilation observed during HUT suggests the possibility of a more prominent role for the venous vasculature than has previously been recognized. This finding has implications for diseases in which the cerebral venous system is disrupted, such as multiple sclerosis. My results do not support the existence of a minute-to-minute functional relationship between BR and CA and therefore do not support a model whereby neurogenic input to CA originates in the baroreceptors. However, my results do not negate the possibility of such a relationship occurring over shorter timescales. Experiments using VHUT provide limited evidence in support of some component of neurogenic control originating in the cortex, but more work is needed to confirm and clarify this
Neurogenic Control, Cerebral Autoregulation
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