• Mehmet Gazi Boyacı, Usame Rakip, Adem Aslan, Halit Buğra Koca, Esra Aslan, Serhat Korkmaz, and Serhat Yıldızhan.
• Department of Neurosurgery, Afyonkarahisar Health Sciences University Faculty of Medicine, Afyonkarahisar, Turkey. Electronic address: mgazibyc@hotmail.com.
• World Neurosurg. 2019 Jul 1; 127: e376-e388.

BackgroundCerebral vasospasm remains a serious problem affecting morbidity and mortality in patients with subarachnoid hemorrhage (SAH) during neurosurgery. We aimed to demonstrate the role of the transient receptor potential channel and other channels for Ca2+ in the etiology of cerebral vasospasm using 2-aminoethyl diphenylborinate (2-APB) and the effective dose range of an unstudied pharmacological agent, which can limit vasospasm.MethodsWe performed an experimental study using 32 Sprague-Dawley rats divided into 4 groups: sham group (n = 8), SAH group (n = 8), 2-APB group (SAH rats intraperitoneally administered with 0.5 mg/kg 2-APB; n = 8), and 2-APB-2 group (SAH rats intraperitoneally administered with 2 mg/kg 2-APB; n = 8). The rats were sacrificed after 24 hours, and superoxide dismutase, glutathione peroxidase, malondialdehyde, tumor necrosis factor-α, and interleukin-1β in the brain tissue and serum were measured. The histopathological investigation of brain tissue included measurement of the luminal diameter and wall thickness of the basilar artery (BA), and apoptotic cells in the hippocampus were counted after caspase staining.ResultsAutologous arterial blood injection into the cisterna magna caused vasospasm in rats. 2-APB treatment increased the BA wall thickness and reduced the BA lumen diameter, inducing significant vascular changes. 2-APB also alleviated cell apoptosis at 24 hours after SAH.ConclusionIn experimental SAH in rats, 2-APB treatment increased the BA wall thickness and reduced the BA lumen diameter, inducing significant vascular changes. 2-APB also alleviated cell apoptosis at 24 hours after SAH.Copyright © 2019 Elsevier Inc. All rights reserved.

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