POINT-COUNTERPOINTRebuttal from Van Lieshout and SecherPublished Online:01 Oct 2008https://doi.org/10.1152/japplphysiol.90597.2008bMoreSectionsPDF (37 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Neither the “neurovascular unit” (4) nor sympathetic activity to the brain vessels are recorded in humans and we have to rely on indirect evidence to evaluate the importance of sympathetic modulation of cerebral blood flow (CBF), e.g., during treatment of patients with a low blood pressure. Cerebral autoregulation describes that CBF stays relatively stable within a mean arterial pressure (MAP) of ∼60–150 mmHg, while a lower pressure reduces CBF and a high MAP increases CBF (6). Thus hypotension may challenge CBF as soon as MAP decreases below the lower limit of cerebral autoregulation. As illustrated (9), the central blood volume and, therefore, cardiac output (CO) adversely influence the lower limit of cerebral autoregulation and maybe in contrast to Strandgaard and Sigurdsson (7), we consider that in situations where central blood volume is critically reduced, CBF is not being prioritized. Under those conditions cerebral perfusion declines to about one-half the normal value and cerebral oxygenation is lowered by more than 10% with development of (pre)syncopal symptoms, while a Bezold-Jarish-like reflex concurrently increases muscle blood flow and oxygenation (5, 8) as first described by Barcroft et al. (1).Accordingly, when there is a need to pharmacologically elevate a low blood pressure, is it then sufficient to increase MAP or should CO also be elevated? As CO is, in general, not taken into account when regulation of CBF is described (6), it may be considered to be sufficient to increase MAP with the administration of an α-adrenergic agonist like phenylephrine. On the other hand, if the cerebral vessels were significantly innervated by α-adrenergic receptors, the effects of α-receptor activation restoring MAP would be considered not being limited to the peripheral vasculature but also to encompass the brain.What we find is that administration of phenylephrine, when used to treat arterial hypotension, not only reduces CO, but also cerebral perfusion and oxygenation even when administered to a normal subject, elevating MAP to beyond what is considered the upper limit of cerebral autoregulation. Thus phenylephrine elicits cerebral vasoconstriction, illustrating a potential influence for the sympathetic nervous system in the regulation of CBF (3). Therefore phenylephrine is not the drug of choice for treatment of a hypotensive patient if the aim is to secure CBF.Sympathetic activity to the cerebral circulation affecting CBF under certain circumstances cannot be ignored and the strategy for treatment of hypotension should include the normalization of CO in so-called individualized goal-directed volume therapy (2) to efficiently enhance CBF and cerebral oxygenation.REFERENCES1 Barcroft H, Edholm OG, McMichael J, Sharpey-Schafer EP. Posthaemorrhagic fainting study by cardiac output and forearm flow. Lancet 243: 489–491, 1944.Crossref | Google Scholar2 Bundgaard-Nielsen M, Holte K, Secher NH, Kehlet H. Monitoring of perioperative fluid administration by individualized goal-directed therapy. Acta Anaesthesiol Scand 51: 331–340, 2007.Crossref | ISI | Google Scholar3 Cassaglia PA, Griffiths RI, Walker AM. Sympathetic nerve activity in the superior cervical ganglia increases in response to imposed increases in arterial pressure. Am J Physiol Regul Integr Comp Physiol 294: R1255–R1261, 2008.Link | ISI | Google Scholar4 Hamel E. Perivascular nerves and the regulation of cerebrovascular tone. J Appl Physiol 100: 1059–1064, 2006.Link | ISI | Google Scholar5 Madsen PL, Secher NH. Near-infrared oximetry of the brain. Prog Neurobiol 58: 541–560, 1999.Crossref | PubMed | ISI | Google Scholar6 Poulson OB, Strandgaard S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 2: 161–192, 1990.PubMed | Google Scholar7 Strandgaard S, Sigurdsson ST. Counterpoint: Sympathetic activity does not influence cerebral blood flow. J Appl Physiol; doi:10.1152/japplphysiol.90597.2008aLink | ISI | Google Scholar8 Van Lieshout JJ, Wieling W, Karemaker JM, Secher NH. Syncope, cerebral perfusion, oxygenation. J Appl Physiol 94: 833–848, 2003.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 105Issue 4October 2008Pages 1367-1367 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.90597.2008bHistory Published online 1 October 2008 Published in print 1 October 2008 Metrics