Does NO regulate the cerebral blood flow response in hypoxia?

Abstract

To study whether nitric oxide (NO) affects the CBF response to hypoxic and carbon monoxide (CO) hypoxia. We incrementally reduced arterial oxygen content in rats, by decreasing the concentration of inspired oxygen (20 rats) or by repeated CO inhalation (20 rats), and measured local CBF using the hydrogen clearance method. Ten animals of each group received 80 mg/kg NO synthase (NOS) inhibitor N-monomethyl-L-arginine intravenously prior to hypoxia, while 10 rats served as controls. Inhibition of NOS decreased mean CBF by 30% and increased cerebrovascular resistance by 70%. Under hypoxic hypoxia, mean oxygen reactivity of CBF (relative change of CBF to a change of arterial oxygen content) was 7.8%/vol% in control animals and 3.3%/vol% after NOS inhibition (P < 0.02). Under CO hypoxia, mean oxygen reactivity was 7.3%/vol% in control animals and 5.1%/vol% after NOS inhibition (P < 0.05). Inhibition of NOS diminished significantly the cerebral vasodilatory response during hypoxic hypoxia (P < 0.05) but only to a lesser extent during CO hypoxia. These observations suggest that NO is involved in cerebral oxygen vasoreactivity, particularly in severe hypoxia.