Abstract TP336: Renal Denervation Reduces Cerebral Vasospasm After Subarachnoid Hemorrhage in Rats

Background and Purpose: Renal denervation (RD) was shown to have several organ protective effects via suppression of sympathetic nerve activation. As sympathetic nerve activation is involved in the pathogenesis of subarachnoid hemorrhage (SAH), RD can be a good candidate treatment to improve SAH prognosis. In this study, we hypothesized that RD reduced early brain injury and cerebral vasospasm (CVS) in SAH rats, both of which were major prognostic factors of SAH. Methods: Sprague-Dawley rats were divided into 3 groups: (1) Sham operation, (2) SAH+vehicle, and (3) SAH+RD. Bilateral RD were performed at 60 minutes after SAH induction. Twenty-four hours after SAH, we examined the effect of RD on the blood pressure (BP), neurologic score (NS), cerebral blood flow (CBF), brain water content (BWC),and diameter of basilar artery (BA). Then,the cytotoxic changesand sympathetic nerve activation were evaluatedby immunohistochemistry and western blot. Finally, serum angiotensin II which is one of the predictor of sympathetic nerve activation was measured by ELISA. Results: Although RD decreased elevated BP after SAH, the values of CBF were similar among the 3 groups. RD didn’t show significant improvement of NS and BWC, whereas it significantly prevented CVS. In BA, theexpression levels ofphosphorylated Extracellular Signal-regulated Kinase, Tumor Necrosis Factor-α, Matrix metalloproteinase-9, p22-phagocytic oxidase, and infiltration of macrophages were upregulated by SAH, but they were significantly reduced by RD. In the paraventricular nucleus (PVN) of hypothalamus which are one of the important nucleuses for sympathetic nerve activation, the increased expression of dopamine β-hydroxylase and reactive astrocytes by SAH were significantly suppressed by RD.Moreover,RD significantly decreased serum angiotensin II which were elevated after SAH. Conclusions: The present study demonstrated that RD reduced CVS after SAH and it may be came from suppression of sympathetic nerve activation.