Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Jul;31(7):e13596.
doi: 10.1111/nmo.13596. Epub 2019 Apr 14.

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

Affiliations

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

Bo Zhang et al. Neurogastroenterol Motil. 2019 Jul.

Abstract

Background: 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.

Methods: 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.

Key results: (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).

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

Keywords: autonomic function; gastric motility; gastric slow waves; neuromodulation; spinal cord stimulation.

PubMed Disclaimer

Conflict of interest statement

DISCLOSURE

The authors declare that they have no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Typical tracings of gastric slow waves after the meal. A, Recording of 3 min gastric slow waves at baseline. B, Recording of dysrhythmia 0–3 min after glucagon injection. C, Recording of 0–3 min slow waves after glucagon injection with SCS
FIGURE 2
FIGURE 2
Gastric slow waves during different recording periods in the glucagon and glucagon + SCS sessions. Glucagon decreased the % N GSW (A) and increased % bradygastria (B) and % tachygastria (C) and SCS improved it via suppressing Bradygastria (vs baseline, **P < 0.01)
FIGURE 3
FIGURE 3
Manometric tracing showing the effects of SCS on glucagon-induced hypomotility. A, Recording of 3-min antral contractions at baseline; B, Recording of first 3-min impaired antral contractions right after glucagon injection; C, Recording of 3-min antral contractions after glucagon injection with SCS
FIGURE 4
FIGURE 4
Effects of SCS on postprandial antral motility. Glucagon decreased the gastric contractile MI (B) and AUC (C) and SCS improved it. No significant change of gastric contractile frequency was noted in glucagon or glucagon + SCS session (A). (vs baseline, *P < 0.05; **P < 0.01)
FIGURE 5
FIGURE 5
Effects of SCS on glucagon-induced autonomic function disorders. Glucagon increased LF and LF/HF but decreased HF; SCS increased HF (B) but decreased LF (A) and LF/HF (C). (vs baseline, **P < 0.01)
FIGURE 6
FIGURE 6
Correlation between sympathetic activity and gastric motility during three consecutive 15‐min periods after glucagon without SCS. LF was negatively correlated with % N GSW (A) and gastric motility (B)

Similar articles

References

    1. Enck P, Azpiroz F, Boeckxstaens G, et al. Functional dyspepsia. Nat Rev Dis Primers. 2017;3:17081. - PubMed
    1. Venara A, Neunlist M, Slim K, et al. Postoperative ileus: Pathophysiology, incidence, and prevention. J Vise Surg. 2016;153:439–446. - PubMed
    1. Sato T, Kitahara F, Nakamura T, Kojima Y, Fujino MA. [Peptic ulcer in patients with diabetes mellitus]. Nihon Rinsho. 2002;60:1580–1584. - PubMed
    1. O’Grady G, Wang TH, Du P, Angeli T, Lammers WJ, Cheng LK. Recent progress in gastric arrhythmia: pathophysiology, clinical significance and future horizons. Clin Exp Pharmacol Physiol. 2014;41:854–862. - PMC - PubMed
    1. van Helden DF, Laver DR, Holdsworth J, Imtiaz MS. Generation and propagation of gastric slow waves. Clin Exp Pharmacol Physiol. 2010;37:516–524. - PubMed

Publication types