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Summary: Disturbances in the nitric oxide (NO) vasodilatory pathway have been implicated in acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). The authors hypothesize that blood released during SAH leads to vasocon striction by scavenging NO and limiting its availability. This was tested by measuring the major NO metabolites nitrite and nitrate in five different brain regions before and after experi mental SAH. The basal NO metabolites levels were as follows (mean ± SO, f.Lmol/mg wet weight): brain stem, 0.14 ± 0.07; cerebellum, 0.12 ± 0.08; ventral convexity cortex, 0.22 ± 0.15; dorsal convexity cortex, 0.16 ± 0.11; and hippocampus, 0.26 ± 0.17. In sham-operated animals, no effect of the nitric oxide synthase (NOS) inhibitor L G -nitro-L-arginine-methyl-ester (30 mg/kg) was found on NO metabolites 40 minutes after admin istration, but a significant decrease was seen after 120 minutes.Cerebral blood flow decreases acutely and ischemic injury occurs after subarachnoid hemorrhage (SAH) in both experimental and clinical studies. Cerebral arteries have been shown to respond to SAH with a biphasic constriction. An acute constriction begins minutes after the bleed, and delayed vasospasm begins 48 hours later . Although the significance of de layed vasospasm is recognized (Sobey and Faraci, 1998 604The NO metabolites decreased significantly 10 minutes after SAH in all brain regions except for hippocampus, and recov ered to control levels in cerebellum at 60 minutes and in brain stem and dorsal cerebral cortex 180 minutes after SAH, while remaining low in ventral convexity cortex. Nitrite recovered completely in all brain regions at 180 minutes after SAH, whereas nitrate remained decreased in brain stem and ventral convexity cortex. Our results indicate that SAH causes acute decreases in cerebral NO levels by a mechanism other than NOS inhibition and provide further support for the hypothesis that alterations in the NO vasodilatory pathway contribute di rectly to the ischemic insult after SAH.

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Intradural hemangiopericytomas, although rare, cannot be differentiated from other, more benign tumors. Spinal hemangiopericytomas ideally should be resected en bloc to reduce operative blood loss and potentially increase disease-free survival time. Despite total surgical resection of these benign-seeming lesions, the high recurrence rate mandates close follow-up and consideration of adjuvant therapy.