Abstract
BackgroundNeuroinflammation is implicated in cerebral vasospasm and brain injuries after subarachnoid hemorrhage (SAH). In addition to classical neuroinflammation with increased inflammatory cytokines, a sterile neurogenic inflammation characterized by release of potent vasoactive neuropeptides may be responsible for brain injuries after SAH. Sympathetic discharges from superior cervical ganglion contribute to vasoconstriction of cerebral arteries Thus, we investigated the effects of surgical cervical sympathectomy on the neurogenic inflammatory neuropeptides shortly after SAH induction in a model of SAH in rats. MethodsMale Wistar rats were divided into 4 groups: control; was not touched, saline group; 300 μl of saline was injected into prechiasmatic cistern, SAH+Sham group; 300 μl of autologous blood was injected to induce subarachnoid hemorrhage into prechiasmatic cistern; SAH+Symp group; the left cervical sympathetic branch was surgically removed after the induction of SAH. Levels of neuropeptides CGRP, SP and VIP which are responsible for neurogenic inflammation, in plasma, trigeminal ganglion, brainstem and brain tissue were measured by ELISA. In addition, c-fos expression as a marker of neuronal activation in the trigeminal nucleus caudalis (TNC) was determined by immunohistochemical staining. ResultsSAH significantly increased c-fos expression in the TNC, as well as CGRP, SP and VIP concentrations in plasma and trigeminal ganglion neurons, and also CGRP and SP concentrations in the brainstem. Cervical sympathectomy application significantly reduced the increases in these parameters induced by SAH. ConclusionsOur findings suggest that cervical sympathectomy treatment may prevent early brain injury by modulating SAH-induced neurogenic inflammatory neuropeptides such as CGRP, SP and VIP, and improve the quality of life in survivors following SAH.
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