O-038 Sympathetic nervous system activation causes cerebral perfusion deficit and cerebral vasoconstriction in Swine

Abstract

<h3>Introduction</h3> Cerebral vasospasm occurs from reversible narrowing of blood vessels, leading to stroke and poor patient outcomes following aneurysm rupture and traumatic brain injury. Sympathetic-mediated vasoconstriction from the superior cervical ganglion (SCG) is thought to be a significant contributor to cerebral vasospasm. We sought to demonstrate that activation of SCG can cause ipsilateral cerebral perfusion deficit and vasoconstriction, similar to that of human cerebral vasospasm. Furthermore, we aimed to show that inhibition of SCG can reverse the effects sympathetic-mediated vasoconstriction. <h3>Methods</h3> SCG was surgically identified in swine and was electrically stimulated to achieve sympathetic activation. CT perfusion was used to assess for changes in cerebral blood flow (CBF) and cerebral blood volume (CBV). Syngo.via software was used to quantify perfusion changes. Digital subtraction angiography was used to assess for changes in vessel diameter. Our institution’s Picture Archiving and Communications System (PACS) was used to measures vessel diameters. <h3>Results</h3> SCG activation reduced mean ipsilateral CBF and CBV by 20–30% compared to its contralateral unaffected side (p&lt;0.001) (figure 1). SCG stimulation also decreased ipsilateral mean vessel diameters of ascending pharyngeal artery (APA), anterior middle cerebral artery (aMCA) and anterior cerebral artery (ACA) by 35–45% compared to baseline (p&lt;0.01) (figure 1). Injecting lidocaine to SCG inhibited the effects of SCG stimulation, returning perfusion and vessel diameter back to baseline. <h3>Conclusion</h3> In swine, electrical stimulation of SCG results in reproducible cerebral vasoconstriction and perfusion deficit comparable to cerebral vasospasm. This can be inhibited by prior local anesthetic injection into the SCG, a possible therapeutic target for cerebral vasospasm. <h3>Disclosures</h3> <b>W. Kim:</b> 1; C; NIH Research Education Programs (R25). <b>M. Samarage:</b> None. <b>D. Zarrin:</b> None. <b>K. Goel:</b> None. <b>J. Johnson:</b> None. <b>A. Wang:</b> None. <b>G. Colby:</b> 1; C; Casa Colina Foundation research grant.