Stellate ganglia stimulation counteracts vagal stimulation by significantly increasing heart rate and blood pressure.

BACKGROUND

Vasovagal syncope (VVS) is the leading cause of syncope. The most frequent mechanism is that of a cardioinhibitory response, vasodepressor response, or mixture of both. Neural stimulation that negates or overcomes the effects of vagal tone may be used as a treatment strategy for VVS.

METHODS

Six male canines were studied. Stimulation (10-Hz, 2 ms pulse duration, 2 min duration) of the cervical vagus (CV), thoracic vagus (TV), and stellate ganglia (SG) was performed using needle electrodes at 3 V, 5 V, and 10 V output. SG stimulation at an output of 10 V overlaying TV stimulation at the same output was performed. Heart rate (HR), blood pressure (BP), and cardiac output (CO) were measured before, during, and after stimulation.

RESULTS

Right cervical vagal stimulation was associated with significant hemodynamic changes. HR, SBP, and DBP were reduced (107 ± 16 vs. 78 ± 15 bpm [P < 0.0001], 116 ± 24 vs. 107 ± 28 mmHg [P = 0.002] and 71 ± 18 vs. 58 ± 20 mmHg [P < 0.0001]), respectively, while left cervical vagal stimulation had minimal changes. CV stimulation was associated with greater hemodynamic changes than TV stimulation. Left and right SG stimulation significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR at 5 V and 10 V, which could be observed within 30 s after stimulation. An output-dependent increase in hemodynamic parameters was seen with both left and right SG stimulation. No difference between left and right SG stimulation was seen. SG stimulation overlay significantly increased HR, BP, and CO from baseline vagal stimulation bilaterally.

CONCLUSIONS

Stellate ganglia stimulation leads to increased HR and BP despite significant vagal stimulation. This may be exploited therapeutically in the management of vasovagal syncope.