Inhibition of neuronal nitric oxide synthase improves microregional O 2 balance in cerebral ischemia-reperfusion

• Published in: Neurological research (New York) 2015-06, p.151218061524001
• Main Authors: Chi, Oak Z, Rah, Kang H, Barsoum, Sylviana, Liu, Xia, Weiss, Harvey R
• Format: Article
• Language: English
• ISSN: 0161-6412; 1743-1328
• DOI: 10.1179/1743132815Y.0000000062

Objectives Return of regional cerebral blood flow (rCBF) in focal cerebral ischaemia may not ensure proper distribution of blood flow to meet metabolic demand. This study was performed to determine how inhibition of neuronal nitric oxide synthase (NOS) during ischaemia-reperfusion would affect microregional O supply/consumption balances and their variation. Methods Twenty minutes before middle cerebral artery (MCA) occlusion, a NOS inhibitor 7-nitroindazole (7-NI) 50 mg/kg ip (7-NI group) or vehicle (control group) was administered. At 1 hour of ischaemia and 2 hours of reperfusion, rCBF, the size of cortical infarct and arteriolar and venular O saturations (20-60 μm in diameter) using cryomicrospectrophotometry were determined. Results Ischaemia-reperfusion decreased the average venular O saturation and the ratio of O supply/consumption. But, 7-NI treatment improved the average O supply/consumption ratio and venular O saturation (57.6 ± 1.3 vs 52.0 ± 3.8%) in ischaemia-reperfusion. The heterogeneity of venular O saturations reported as coefficient of variation (CV = 100 × SD/mean) was much smaller in the 7-NI than the control group (8.8 vs 15.5). The number of veins with low O saturation (