Role of nitric oxide in regulating cerebrocortical oxygen consumption and blood flow during hypercapnia

Ildiko Horvath, Norbert T. Sandor, Zoltan Ruttner, Alan C. McLaughlin

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The effect of the nitric oxide (NO) synthase inhibitor N(ω)-nitro-L- arginine methyl ester (L-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (P(a)CO2 ~ 60 mm Hg and P(a)CO2 ~ 90 mm Hg) was investigated in ketamine- anesthetized rats. CBF was calculated using the Kety-Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect on either CMRO2 or CBF under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.

Original languageEnglish
Pages (from-to)503-509
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number3
Publication statusPublished - May 1994



  • Cerebral blood flow
  • Cerebral oxygen consumption
  • Hypercapnia
  • L-NAME
  • Nitric oxide

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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