Changes in NADPH-d/nitric oxide synthase perivascular networks in rat cerebral cortex after autologous blood injection in the subarachnoid spaces

Nitric oxide (NO) plays multiple roles in the central nervous system. NO producing neurons make perivascular networks with cerebral cortex microvessels and contribute to cerebral cortex vascular tone regulation. The authors analyzed the distribution of neuronal/inducible NO synthase and nicotinamidedinucleotide phosphate diaphorase (NADPH-d) in the rat cerebral cortex after autologous blood injection in the subarachnoid spaces, to understand the role of NO in the pathogenesis of subarachnoid hemorrhage (SAH)-induced cortical damages. Autologous blood was injected in rats into the cisterna magna. Sham-operated rats received saline injections. Animals were killed at different time intervals (6 hours to 1 week) perfused, and their brains were removed for histochemistry and immunohistochemistry. The transverse diameter of the basilar artery was measured. Six to twelve hours after SAH, there were no differences between sham and SAH rats; iNOS staining was absent. Twenty-four hours after SAH, diffuse NADPH-d and nNOS reactivity increased in treated rats and moderate iNOS staining appeared without basilar diameter variations. Forty-eight hours, 72 hours to 1 week after SAH, NADPH-d/nNOS labeling changed in treated animals when compared with controls; iNOS immunoreactivity was intense. Basilar diameter suggested vasospasm. These results suggest a role of neuronal NO in SAH cortical damages and vasospasm. Key words: nitric oxide, subarachnoid hemorrhage, vasospasm, brain injury, NADPH-d