Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow During Hypercapnia

• Published in: Journal of cerebral blood flow and metabolism 1994-05, Vol.14 (3), p.503-509
• Main Authors: Horvath, Ildiko, Sandor, Norbert T., Ruttner, Zoltan, McLaughlin, Alan C.
• Format: Article
• Language: English
• Subjects: Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Blood Pressure - drug effects; Cerebral Cortex - blood supply; Cerebral Cortex - metabolism; Cerebrovascular Circulation - drug effects; Hypercapnia - physiopathology; Male; Medical sciences; NG-Nitroarginine Methyl Ester; Nitric Oxide - antagonists & inhibitors; Nitric Oxide - physiology; Oxygen Consumption; Pneumology; Rats; Respiratory system : syndromes and miscellaneous diseases; Space life sciences
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1994.62

The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 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 CBE 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.