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We performed this study to determine how pretreatment of the ovariectomized rats with 17beta-estradiol could affect blood-brain barrier disruption caused by the vascular endothelial growth factor (VEGF), an important mediator of vascular permeability. Ovariectomized female rats aged twelve to fourteen weeks were used in the study. A 500 micro g 17beta-estradiol 21-day release pellet was implanted in the 17beta-estradiol group, and a vehicle pellet was implanted in the control group 21 days before the experiments. We performed three craniotomies under isoflurane anesthesia to expose cerebral cortices. Normal saline, 10 (- 10)M and 10 (- 9)M VEGF patches were applied on each hole for 30 min. The transfer coefficient (Ki) of (14)C-alpha-amino isobutyric acid and volume of (3)H-dextran (70,000 dalton) distribution were determined to measure the degree of BBB disruption. Ki was increased by 108 % and 138 % with 10 (- 10)M and 10 (- 9)M VEGF respectively after VEGF application in the control group (p < 0.01). However, there was no significant increase in the Ki with the VEGF application in the 17beta-estradiol group, and their values were significantly lower than the corresponding data of the control group (10 (- 10)M: - 55 %, 10 (- 9)M: - 52 %, p <0.05). The volume of dextran distribution in the control group increased by 47 % with VEGF 10 (- 9)M (p < 0.05), whereas there was no significant change in the volume of dextran distribution with VEGF application in the 17beta-estradiol group and the volume was lower than the corresponding volume of the vehicle-treated control group (10 (- 10)M: - 34 %, 10 (- 9)M: -32 %, p < 0.05). In conclusion, our study demonstrated that chronic 17beta-estradiol treatment prevented BBB disruption induced by the VEGF in the ovariectomized rats.

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Vasospasm that occurs after subarachnoid hemorrhage (SAH), despite successful surgical or radiological intervention remains with an ominous prognostic recovery period. 1 We investigated the correlation of S100B protein in CSF and serum with incident of vasospasm and neurological outcome in patients undergoing intracerebral aneurysm clipping. Twenty five patients were enrolled. All patients received combined anesthetic techniques. Brain protection was provided by isoflurane. A CSF sample (2 cc) and blood sample (5 cc) were drawn 3 times (before skin incision, 30 minutes and 24 hours after clipping). Patients were followed for the incidence of vasospasm in Neurosurgical Intensive Care Unit and the neurological status at discharged was assessed using Glasgow Outcome Scale. Compared with baseline level (at 0 minute) we found that early changes in CSF S100 B level at 30 minutes significantly correlate with vasospasm (P = 0.005, sensitivity 90% and specificity 90%) but the correlation dissipated at 24 hours. In addition, early changes in S100B in CSF at 30 minutes significantly correlate with neurological outcome (P = 0.003). The relationship persisted at 24 hours (P , 0.011). In Serum we found no significant correlation between S100B at 30 minutes or 24 hours with either vasospasm or neurological outcome. We conclude that changes of S100B level in CSF in patients undergoing intracerebral aneurysm clipping surgery are strongly correlated with vasospasm and can be a reliable diagnostic tool to identified patients who are endangered with evolving vasospasm after a successful securing aneurysm surgery. Reference: 1. Pluta RM. Delayed cerebral vasospasm and nitric oxide: review, new hypothesid, and proposed treatment.

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