Superior Cervical Ganglion Stimulation Results in Potent Cerebral Vasoconstriction in Swine

Abstract

Introduction— Sympathetic activity from the superior cervical ganglion (SCG) has been shown to cause cerebral
hypoperfusion in swine, similar to that seen with clinical cerebral vasospasm. Although the mechanism of such
perfusion deficit has been speculated to be from pathologic cerebral vasoconstriction, the extent of sympathetic
contribution to vasoconstriction has not been well-established.
Objective— We aimed to demonstrate that SCG stimulation in swine leads to significant cerebral vasoconstriction
on digital subtraction angiography (DSA). Additionally, we aimed to show that inhibition of SCG can mitigate the
effects of sympathetic-mediated cerebral vasoconstriction.
Methods— Five SCGs were surgically identified in Yorkshire swine and were electrically stimulated to achieve
sympathetic activation. DSA was performed to measure and compare changes in cerebral vessel diameter. Syngo
iFlow was also used to quantify changes in contrast flow through the cerebral and neck vessels.
Results— SCG stimulation resulted in 35-45% narrowing of the ipsilateral ascending pharyngeal, anterior middle
cerebral and anterior cerebral arteries. SCG stimulation also decreased contrast flow through ipsilateral ascending
pharyngeal, internal carotid and anterior cerebral arteries as seen on iFLow. These effects were prevented with prior
SCG blockade. Minimal vessel caliber changes were seen in the posterior cerebral, posterior middle cerebral and
internal carotid arteries with SCG stimulation.
Conclusion— SCG stimulation results in significant luminal narrowing and reduction in flow through various
intracranial arteries in swine. The results of sympathetic hyperactivity from the SCG closely models cerebral
vasoconstriction seen in human cerebral vasospasm. SCG inhibition is a potential promising therapeutic approach to
treating cerebral vasospasm.