• Ruibin Zheng, Lei Qin, Songbai Li, Ke Xu, and Haiyang Geng.
• Departments of Radiology, First Affiliated Hospital of China Medical University, 155 Nanjing N St, Shenyang, 110001, Liaoning Province, People's Republic of China.
• Acta Neurochir (Wien). 2014 Mar 1;156(3):527-33.

BackgroundVasospasm of both large and small parenchymal arteries may contribute to the occurrence of delayed ischemic neurological deficits, and nitric oxide(NO) is an important mediators in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). We used a rabbit two-hemorrhage model to investigate changes in plasma NO after SAH, and the relationship between NO and brain microcirculation.MethodsSAH was induced in rabbits and a control group was sham operated. There were 32 rabbits in each group that survived the second operation, and they were randomly assigned to four groups of eight rabbits each for follow-up assessments on Days 1, 4, 7, or 14, respectively. Cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) were calculated at six regions of interest (ROIs): symmetrical areas of the frontal, parietal-occipital, and temporal lobes. Before the contrast CT scan, blood was drawn from the central artery of the ear for measurement of plasma NO.ResultsIn the control group, there was no difference in CBV, CBF, and MTT in the six ROIs, and plasma NO was unchanged. Compared to controls, in the SAH group, CBV decreased slightly in the six ROIs (P > 0.05), frontal lobe CBF decreased, MTT increased (P < 0.05, for both), and NO plasma levels were significantly lower (P < 0.01).ConclusionsThere was a significant correlation between the increase in MTT and the decrease in plasma NO (P < 0.05), We hypothesized that normalization of NO might have a positive influence on brain microcirculation following SAH.

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