7-nitroindazole impedes erythrocyte flow response to isovolemic hemodilution in the cerebral capillary circulation

The role of nitric oxide (NO) in the mechanism of hemodilution-induced cere bral hyperemia is unclear. Based on findings in hypoxemia, the authors hypo thesize that NO of neuronal origin contributes to an increase in velocity o f erythrocytes in the cerebral microcirculation during anemia produced by i sovolemic hemodilution. The change in erythrocyte velocity in cerebrocortic al capillaries was assessed by intravital fluorescence video microscopy. A closed cranial window was implanted over the frontoparietal cortex of barbi turate-anesthetized, ventilated adult rats. Erythrocytes were labeled in vi tro with fluorescein isothiocyanate and infused intravenously, and their ve locity in subsurface capillaries was measured by frame-to-frame image track ing. Arterial blood was withdrawn in increments of 2 mL and replaced by ser um albumin; arterial blood pressure was maintained at control level with an infusion of methoxamine. Erythrocyte velocity increased progressively, rea ching 215% of baseline, as arterial hematocrit was reduced from 45% to 17%. Pretreatment of a separate group of rats with 7-nitroindazole (20 mg/kg in traperitoneally), a relatively selective inhibitor of neuronal NO synthase, abolished the increase in velocity at hematocrits greater than 20%, but th e maximum velocity attained at the lowest hematocrit was similar tu that in the control group. The results suggest that NO from neuronal source may co ntribute to the increase in capillary erythrocyte now during moderate isovo lemic hemodilution.