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POINT-COUNTERPOINT
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 
-adrenergic agonist like phenylephrine. On the other hand, if the cerebral vessels were significantly innervated by -adrenergic receptors, the effects of -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.
REFERENCES
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