“…testinal transit evoked by evisceration and gut manipulation in a dose-dependent manner. These results are consistent with data showing that NK 1-3 antagonists do not affect peristalsis in guinea pig and dog under normal conditions [14,15], whereas they exert a protective action against the inhibition of gastrointestinal motility invoked by colorectal distension or intestinal manipulation [9,16,17]. In contrast, Herrscher showed that the administered combination of NK 1 receptor and CGRP antagonists abolish the protective activity of each agent given separately to prevent the postoperative gastric motility inhibition [18].…”
“…testinal transit evoked by evisceration and gut manipulation in a dose-dependent manner. These results are consistent with data showing that NK 1-3 antagonists do not affect peristalsis in guinea pig and dog under normal conditions [14,15], whereas they exert a protective action against the inhibition of gastrointestinal motility invoked by colorectal distension or intestinal manipulation [9,16,17]. In contrast, Herrscher showed that the administered combination of NK 1 receptor and CGRP antagonists abolish the protective activity of each agent given separately to prevent the postoperative gastric motility inhibition [18].…”
“…Several observations suggest that there is a tonic cholinergic input to the proximal stomach under normal physiological conditions. For instance, in both dogs and humans, atropine reduced the proximal gastric tone during both fasting and gastric balloon distension [1,26,27]. However, Bruley des Varannes et al [28] did not find any significant effect on fasting or postprandial gastric tone in humans treated with atropine, which is similar to the present result in SD rats.…”
The results indicate that WKY rats may have an increased gastric vagal cholinergic drive, which, during distension, masks the relaxing effect of NO-releasing neurons. The findings in WKY rats could be of relevance for functional dyspeptic patients with impaired gastric accommodation to meals.
“…The control of proximal gastric tone is mainly mediated by cholinergic and nitrergic efferent nerves through vagovagal pathways and is based on a balance between the cholinergic contractile and the nitrergic relaxant drive (22)(23)(24). Atropine, as a cholinergic pathway blocker, inhibits the effects of vagal impulses, relaxes the proximal stomach, and reduces fasting proximal gastric tone (25,26). The mechanisms via which rectal distension affects gastric tone are unclear.…”
Rectal distension affects upper GI myoelectrical activity and motility. The aim of this experiment was to investigate the effect of rectal distension on gastric tone, accommodation, and the underlying mechanism. Seven healthy dogs were surgically prepared and studied. Gastric tone and accommodation were assessed with a barostat. In Experiment 1, the effect of rectal distension on gastric tone and accommodation was evaluated; in Experiment 2, rectal distensions with various volumes were randomly applied and its effects on gastric tone were evaluated; and in Experiment 3, the role of the cholinergic pathway in distension-induced gastric relaxation was assessed. The results showed the following. (1) Rectal distension exerted an inhibitory effect on gastric tone, and this response was distension volume-dependent. (2) Postprandial gastric volume was similar in the control (468.6 +/- 24.7 ml) and the distension study (463.2 +/- 17.5 ml). However, rectal distension increased the preprandial gastric volume, and subsequently decreased the extent of gastric accommodation (139.3 +/- 34.7 ml), which was significantly lower than that of the control (383.2 +/- 26.3 ml; P < 0.001). (3) An intravenous bolus of atropine increased the astric volume from the baseline of 89.4 +/- 12.6 ml to 161.5 +/- 9.8 ml (P < 0.01), and subsequent rectal distension further increased this volume, but the overall change was comparable between the control (297.6 +/- 18.7 ml) and the atropine study (312.1 +/- 21.9 ml; P > 0.05). In conclusion, rectal distension inhibits gastric tone in a volume-dependent manner and impairs gastric accommodation. Atropine dose not block the effect of rectal distension on proximal gastric tone, suggesting that the observed effect may not be mediated by cholinergic pathway.
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