Prokinetic effects of spinal cord stimulation and its autonomic mechanisms in dogs

Spinal cord stimulation (SCS) is widely used to treat chronic pain by inhibiting sympathetic activity; however, it is unknown whether it exerts a prokinetic effect on gastric motility. Our aim was to explore effects and possible mechanisms of SCS on glucagon-induced gastric dysmotility and dysrhythmia.

Seven female dogs with electrodes chronically placed on the dorsal column of the spinal cord between T10 and T12 segments were studied in 2 randomized sessions (glucagon + sham-SCS, glucagon + SCS). SCS at T10 using a set of optimized stimulation parameters was performed for 30 minute immediately after glucagon injection. The antral manometry, electrogastrogram, and electrocardiogram were recorded to assess gastric contractions, gastric slow waves (GSW), and autonomic functions, respectively.

(a) Compared to baseline, glucagon decreased antral motility index (MI) (6315 ± 565 vs 3243 ± 775, P < 0.001), reduced the percentage of normal GSW (89 ± 3% vs 58 ± 3%, P < 0.01), and increased sympathetic activity (0.25 ± 0 0.06 vs 0.60 ± 0.07, P < 0.01). (b) The sympathetic activity was negatively correlated with antral MI (r = -0.558; P < 0.01) and the percentage of gastric normal slow wave (r = -0.616; P < 0.01). (c) SCS prevented the glucagon-induced impairment in antral hypomotility (MI: 5770 ± 927 vs 5521 ± 1238, P > 0.05) and GSW abnormalities (% of normal waves: 84 ± 4% vs 79 ± 6%, P > 0.05) and sympathetic activity (0.27 ± 0.03 vs 0.33 ± 0.07, P > 0.05).

Spinal cord stimulation dramatically improves glucagon-induced impairment in gastric contractions and slow waves by inhibiting sympathetic activity.