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This Article Full Text Full Text (PDF) All Versions of this Article: 105/4/1060    most recent 90613.2008v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Peebles, K. C. Articles by Ainslie, P. N. PubMed PubMed Citation Articles by Peebles, K. C. Articles by Ainslie, P. N.

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

Departments of ¹Physiology and ³Medicine, University of Otago, Dunedin; and ²Christchurch Cardioendocrine Research Group, Department of Medicine, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand

Submitted 7 May 2008 ; accepted in final form 8 July 2008

Cerebral blood flow (CBF) is highly regulated by changes in arterial PCO₂ and arterial PO₂. Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO₂), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O₂). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 ± 18 and 150 ± 36 µmol/l at 4% and 8% CO₂, respectively (both P < 0.05). Release of cerebral CNP was also observed during changes in CO₂ (hypercapnia vs. hypocapnia, P < 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: –96 ± 14 µmol/l at 10% O₂ (P < 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO₂-induced CBF changes.

cerebral circulation; nitric oxide; endothelium