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J Appl Physiol 105: 1367-a-1368-a, 2008; doi:10.1152/japplphysiol.90597.2008c
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POINT-COUNTERPOINT

Rebuttal from Strandgaard and Sigurdsson

The review of van Lieshout and Secher (7) relies heavily on studies of cerebral blood flow velocity, which they seem to think is a worthy substitute for real CBF measurements. Based largely on such studies, they argue that the brain takes part in systemic vascular regulation during threatening hypotension. They make it an important point that CBF velocity decreases slightly when changing the body position from supine to upright. This CBF response is independent of blood pressure and is believed by van Lieshout and Secher to be mediated by perivascular sympathetic nerves in the brain. Since the sympathetic nerves surrounding the cerebral vessels do not reach beyond the Virchow-Robin space (2), such cerebral vasoconstriction could only take place in the larger resistance vessels and would be counterbalanced by autoregulatory dilatation further downstream. Hence it is highly unlikely that this vasoconstrictive response is caused by sympathetic activation. One important study on this orthostatic fall in CBF velocity quoted by van Lieshout and Secher is that of Zhang and Levine (8) who measured CBF velocity without and with systemic ganglionic blockade and found no effect of the latter on the orthostatic fall in CBF velocity. Zhang and Levine concluded, as quoted in our Counterpoint, that contrary to their hypothesis, the orthostatic fall in CBF velocity was not mediated by sympathetic perivascular nerves. Surprisingly, van Lieshout and Secher try to revive this hypothesis, claiming that infusion of phenylephrine in the Zhang and Levine experiment would have mimicked sympathetic vasoconstriction. This goes against the general knowledge that vasoactive amines do not penetrate the blood-brain barrier and only influence cerebral resistance vessels from the outside (4). Errors of methodology, as discussed in our Counterpoint, may have influenced some of the head-up tilt studies (3).

Van Lieshout and Secher quote one study in humans, where CBF as measured by single photon emission computed tomography rose following stellate blockade (6). In the study by Skinhøj (5), quoted in our first paper for lack of effect of bladder distension on CBF, {alpha}-adrenergic blockade was also done and did not influence CBF.

Van Lieshout and Secher controversially claim that cardiac output (CO) influences cerebral blood flow independently of blood pressure. To clarify this, CBF autoregulation studies should be carried out with a systemic vasodilator that raises CO along with lowering blood pressure while being pharmacologically inactive in the cerebral circulation (1). The results should be compared with CBF autoregulation studies with ganglionic blockade, which lowers both CO and blood pressure.

REFERENCES

  1. Barry DI, Strandgaard S, Graham DI, Braendstrup O, Svendsen UG, Bolwig TG. Effect of diazoxide-induced hypertension on cerebral blood flow in hypertensive rats. Eur J Clin Invest 13: 201–207, 1983.[Web of Science][Medline]
  2. Hamel E. Perivascular nerves and the regulation of cerebrovascular tone. J Appl Physiol 100: 1059–1064, 2006.[Abstract/Free Full Text]
  3. Jordan J, Shannon JR, Diedrich A, Black B, Cosata F, Robertson D, Biaggioni I. Interaction of carbon dioxide and sympathetic nervous activity in the regulation of cerebral perfusion in humans. Hypertension 36: 383–388, 2000.[Abstract/Free Full Text]
  4. Olesen J. The effect of intracarotid epinephrine, norepinephrine and angiotensin on the regional cerebral blood flow in man. Neurology 22: 978–987, 1972.[Free Full Text]
  5. Skinhøj E. The sympathetic nervous system and the regulation of cerebral blood flow in man. Stroke 3: 711–716, 1972.[Abstract/Free Full Text]
  6. Umeyama T, Kugimiya T, Ogawa T, Kandori Y, Ishizuka A, Hanaoka K. Changes in cerebral blood flow estimated after stellate ganglion block by single photon emission computed tomography. J Auton Nerv Syst 50: 339–346, 1995.[CrossRef][Web of Science][Medline]
  7. Van Lieshout JJ, Secher NH. Point: Sympathetic activity does influence cerebral blood flow. J Appl Physiol; doi:10.1152/japplphysiol.90597.2008.
  8. Zhang R, Levine BD. Autonomic blockade does not prevent reduction in cerebral blood flow velocity in humans. Stroke 38: 1238–1244, 2007.[Abstract/Free Full Text]




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