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https://www.selleckchem.com/products/Nafamostat-mesylate.html OBJECTIVE Vasospasm after subarachnoid hemorrhage (SAH) plays a vital role in the development of delayed cerebral ischemia. Anti-VEGF antibodies, like bevacizumab, may attenuate VEGF- stimulated angiogenesis, reduced vascular cell proliferation, and improve vasospasm after SAH. METHODS Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits in each group group 1 (control); group 2 (subarachnoid hemorrhage); group 3 (subarachnoid hemorrhage + vehicle); and group 4 (subarachnoid hemorrhage + bevacizumab). BEV (5 mg/kg, intraperitoneally) was administered 5 min after the intracisternal blood injection and continued for 72 h once per day in the same dose for group 4. Animals were sacrificed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS VEGF is associated with the narrowing of the basilar artery. Treatment with BEV statistically significantly increased the cross-sectional area of the basilar artery when compared to the SAH and the vehicle groups. Basilar artery wall thicknesses in the BEV group was statistically significant smaller than in the SAH and vehicle groups. The hippocampal degeneration scores for the BEV and control groups were similar and significantly lower than those for the SAH and vehicle groups. CONCLUSION Cellular proliferation and subsequent vessel wall thickening is reason to delayed cerebral ischemia and deterioration of the neurocognitive function. Intraperitoneal administration of bevacizumab was found to attenuate cerebral vasospasm and prevent delayed cerebral ischemia and improve neurocognitive function after subarachnoid hemorrhage in rabbits. INTRODUCTION In recent decades there has been a significant expansion of neurosurgical capabilities in low-and-middle income countries and particularly in Southeast Asia.

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