• Peiliang Li, Neeraj Chaudhary, Joseph J Gemmete, B Gregory Thompson, Ya Hua, Guohua Xi, and Aditya S Pandey.
• Department of Neurosurgery, University of Michigan, Ann Arbor, MI, USA.
• Acta Neurochir. Suppl. 2016 Jan 1; 121: 331-4.

AbstractEarly brain injury and hydrocephalus (HCP) are important mediators of poor outcome in subarachnoid hemorrhage (SAH) patients. We aim to understand the development of HCP and subependymal cellular injury after intraventricular injection of noncellular human SAH cerebrospinal fluid (CSF) into rat ventricles. Two-hundred microliters of noncellular CSF from SAH patients or normal controls were injected into the right lateral ventricle of seven adult male Sprague-Dawley rats. Propidium iodide (PI) was simultaneously injected to detect necrotic cellular death. Rats were then sacrificed 24 h after surgery and the brain specimens were cut and stained for heme oxygenase 1 (HO-1), an oxidative stress marker. We found that the ventricular area at the bregma level in the CSF injection group was significantly larger than that in the control group (p < 0.05). The periventricular tissue in the CSF injection group had significantly more necrotic cell death as well as HO-1 expression as compared with the control group (p < 0.05). In conclusion, injection of SAH patients' CSF into the rat ventricle leads to HCP as well as subependymal injury compared with injection of control CSF.

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