Pharmacological Regulation of Postprandial Gastrointestinal Motility by Glucagon in Conscious Dogs.

Shimatani, Tomohiko

doi:10.1540/jsmr.33.187

Cited by 1 publication

(1 citation statement)

References 31 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exogenously administered glucagon inhibits gastrointestinal motility in humans and dogs (27,34). Glucagon inhibits the postprandial elevation of the serum gastrin concentration and thus inhibits postprandial antral motility (31). Because of this, glucagon is frequently used as a pharmacological agent to provide temporary inhibition of gastrointestinal movements.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic potential of synchronized gastric electrical stimulation for gastroparesis: enhanced gastric motility in dogs

Zhu¹,

Sallam²,

Chen³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The aim of this study was to determine the effects and mechanism of synchronized gastric electrical stimulation (SGES) on gastric contractions and gastric emptying. The first experiment was designed to study the effects of SGES on antral contractions in four randomized sessions. Sessions 1 (control) and 2 (atropine) were performed in the fasting state, composed of three 30-min periods (baseline, stimulation, and recovery). Sessions 3 (control) and 4 (SGES performed during 2nd 20-min period) were performed in the fed state, consisting of two 20-min periods; glucagon was injected after the first 20-min recording. The second experiment was designed to study the effect of SGES on gastric emptying and consisted of two sessions (control and SGES). SGES was delivered with train duration of 0.5–0.8s, pulse frequency of 40 Hz, width of 2 ms, and amplitude of 4 mA. We found that 1) SGES induced gastric antral contractions in the fasting state. The motility index was 1.3 ± 0.5 at baseline and 6.1 ± 0.7 ( P = 0.001) during SGES. This excitatory effect was completely blocked by atropine. 2) SGES enhanced postprandial antral contractions impaired by glucagon. 3) SGES significantly accelerated glucagon-induced delayed gastric emptying. Gastric emptying was 25.5 ± 11.3% without SGES and 38.3 ± 10.7% with SGES ( P = 0.006 vs. control). This novel method of SGES induces gastric antral contractions in the fasting state, enhances glucagon-induced antral hypomotility in the fed state, and accelerates glucagon-induced delayed gastric emptying. The effect of SGES on antral contractions is mediated via the cholinergic pathway.

show abstract

Section: Discussionmentioning

confidence: 99%