Abstract
Sphenopalatine ganglion stimulation activates perivascular vasodilatory nerves in the ipsilateral anterior circle of Willis. This experiment tested whether stimulation of the ganglion could reverse vasospasm and improve cerebral perfusion after subarachnoid hemorrhage (SAH) in monkeys. Thirteen cynomolgus monkeys underwent baseline angiography followed by creation of SAH by placement of autologous blood against the right intradural internal carotid artery, the middle cerebral artery (MCA), and the anterior cerebral artery. Seven days later, angiography was repeated, and the right sphenopalatine ganglion was exposed microsurgically. Angiography was repeated 15 minutes after exposure of the ganglion. The ganglion was stimulated electrically 3 times, and angiography was repeated during and 15 and 30 minutes after stimulation. Cerebral blood flow (CBF) was monitored using laser Doppler flowmetry, and intracranial pressure (ICP) was measured throughout. The protocol was repeated again. Evans blue was injected and the animals were killed. The brains were removed for analysis of water and Evans blue content and histology. Subarachnoid hemorrhage was associated with significant vasospasm of the ipsilateral major cerebral arteries (23% ± 10% to 39% ± 4%; p < 0.05, paired t-tests). Exposure of the ganglion and sham stimulation had no significant effects on arterial diameters, ICP, or CBF (4 monkeys, ANOVA and paired t-tests). Sphenopalatine ganglion stimulation dilated the ipsilateral extracranial and intracranial internal carotid artery, MCA, and anterior cerebral artery compared with the contralateral arteries (9 monkeys, 7% ± 9% to 15% ± 19%; p < 0.05, ANOVA). There was a significant increase in ipsilateral CBF. Stimulation had no effect on ICP or brain histology. Brain water content did not increase but Evans blue content was significantly elevated in the MCA territory of the stimulated hemisphere. Sphenopalatine ganglion stimulation decreased vasospasm and increased CBF after SAH in monkeys. This was associated with opening of the blood-brain barrier.
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