to the editor:We appreciate the interest generated in possible sympathetic influences on cerebral blood flow (CBF) that are well established for other parts of the circulation. In particular, we appreciate the notion by Poulson and Knudsen (see Ref. 2) that the lower limit of cerebral autoregulation depends on sympathetic activity with a reduction in CBF even at an arterial pressure level close to normal when sympathetic activity is high in response to simulated hemorrhage as depicted in Fig. 1. We take this observation of variation in the lower limit of cerebral autoregulation from 40 to 80 mmHg to indicate that blood pressure during anesthesia and in the intensive care is often insufficient to secure CBF and cerebral oxygenation. Cerebral oxygenation is readily monitored by near infrared spectroscopy as established by arterial oxygen saturation and pulse oxymetry comparisons (2). We accept that the mechanism responsible for a sympathetic restrain on CBF remains to be established. We provided evidence that a low central blood volume and cardiac output seem important, but the trigger may well be stroke volume or pulse pressure and, thereby, enact beat-to-beat variations in distension of the arterial baroreceptor area as elegantly demonstrated by Ead et al. (1). We do hope that the debate on sympathetic influence on CBF inspires the elucidation of the relevant trigger mechanisms for sympathetic control of CBF and creates a basis for securing CBF and cerebral oxygenation in intensive care medicine currently associated with significant death rates.
- Copyright © 2008 the American Physiological Society