NO contributes to neurohypophysial but not other regional cerebral fluorocarbon-induced hyperemia in cats.

The large increase in cerebral blood flow (CBF) after fluorocarbon (FC)-exchange transfusion is thought to be caused by low oxygen content, decreased viscosity, or direct vasodilatory effect of the FC perfusate. The aim of this study was to determine whether nitric oxide (NO)-mediated vasorelaxation is increased in FC-perfused hemoglobin (Hb)-free cats because NO is not scavenged by Hb. We measured regional CBF with radiolabeled microspheres in three groups of anesthetized mechanically ventilated cats. The first group [FC + N ω-nitro-l-arginine methyl ester (l-NAME); n = 7] underwent a complete FC-exchange transfusion with FC-43 and subsequent nitric oxide synthase (NOS) inhibition with l-NAME (10 mg/kg iv) followed by l-arginine (100 mg/kg iv). A second group (FC + saline; n = 6) underwent an identical protocol, but NOS was not antagonized (saline iv). In a third group (blood + l-NAME; n = 7), cats were not FC exchanged but NOS was inhibited. In a separate cohort of four FC-perfused cats, NOS activity in brain tissue samples was reduced to 26% of control after NOS inhibition. FC-exchange transfusion nearly doubled hemispheric blood flow in both FC-exchanged groups, whereas it was constant in the blood + l-NAME group. These increases in regional CBF (hemispheres, brain stem, cerebellum, thalamus, and white matter) were not reversed by inhibition of NOS, except in the neurohypophysis, wherel-NAME reduced blood flow to levels comparable to values in the blood +l-NAME group. In summary, increases in regional CBF after total FC-exchange transfusion are not caused by a lack of NO scavenging, with the exception of neurohypophysis. These findings suggest an increased vasorelaxation in neurohypophysis of FC-perfused and Hb-free cats caused by unscavenged NO, but this mechanism does not play a major role in FC-related CBF increases in the rest of the cerebral circulation.