NEURONAL NO PROMOTES CEREBRAL CORTICAL HYPEREMIA DURING CORTICAL SPREADING DEPRESSION IN RABBITS

Temporary elevations in cortical cerebral blood flow (CBF) accompany c ortical spreading depression (CSD) in anesthetized animals. We tested the hypothesis that nitric oxide (NO) is an important promotor of CSD- induced cortical hyperemia in urethan-anesthetized rabbits. CBF was me asured at four time points by administration of 15-mu m microspheres w ith the reference withdrawal technique. Intravenous administration of the nonspecific NO synthase (NOS) inhibitor N-omega-nitro-L-arginine i ncreased mean arterial blood pressure and resting cerebrovascular resi stance and attenuated CSD-induced hyperemia. Cortical CBF before intra peritoneal 7-nitroindazole (7-NI), a neuronal NOS inhibitor, was 42 +/ - 8 and 124 +/- 19 ml . 100 g(-1). min(-1) at baseline and during CSD, respectively (P < 0.05 by repeated-measures analysis of variance). Af ter 7-NI administration, mean arterial blood pressure, CBF, and cerebr ovascular resistance were unchanged from baseline values; cortical CBF was 38 +/- 4 and 90 +/- 8 ml . 100 g(-1). min(-1) post-7-NI at rest a nd during a second CSD, respectively. Similar to N-omega-nitro-L-argin ine, 7-NI decreased the cortical hyperemic response during CSD (P < 0. 05 by repeated-measures analysis of variance). We conclude that neuron al NOS promotes the temporary cortical hyperemia observed during CSD.