De Ponti F, Azpiroz F, Malagelada J R
Am J Physiol. 1987 May;252(5 Pt 1):G595-601. doi: 10.1152/ajpgi.1987.252.5.G595.
Using a newly developed gastric barostat, we studied the effect of duodenal distention on gastric tone in a chronic canine model. In the conscious, fasted dogs, duodenal distention for 15 s consistently induced a marked gastric relaxation (delta intragastric volume = 226 +/- 23 ml). This response could be induced repeatedly without evidence of fatigue. Neither bethanechol nor combined phentolamine and propranolol infused intravenously had any significant effect on gastric relaxation in response to duodenal distention. To investigate the pathway of this duodenogastric mechanism, in four dogs we isolated the vagal nerves at the supradiaphragmatic level within an implanted cooling jacket. During intravenous infusion of bethanechol (used as a cholinergic background to maintain base-line gastric tone), supradiaphragmatic vagal blockade by cooling abolished the gastric relaxatory response to duodenal distention (delta intragastric volume = 11 +/- 5 ml during vagal blockade vs. 194 +/- 36 after vagal rewarming; P less than 0.05). This effect of acute and reversible vagal blockade by cooling was also mimicked by bilateral surgical vagotomy. We conclude that a nonadrenergic, noncholinergic mechanism participates in gastric relaxation induced by duodenal distention. This mechanism is mediated by the vagus nerve.
我们使用一种新开发的胃内压测定仪,在慢性犬模型中研究十二指肠扩张对胃张力的影响。在清醒禁食的犬中,十二指肠扩张15秒持续诱发明显的胃松弛(胃内体积变化量 = 226 ± 23 ml)。这种反应可反复诱发且无疲劳迹象。静脉注射氨甲酰甲胆碱以及酚妥拉明与普萘洛尔联用,对十二指肠扩张引起的胃松弛均无显著影响。为研究这种十二指肠 - 胃机制的途径,我们在4只犬中,于植入的冷却套内将膈上水平的迷走神经分离。在静脉输注氨甲酰甲胆碱(用作胆碱能背景以维持基线胃张力)期间,通过冷却进行膈上迷走神经阻滞消除了对十二指肠扩张的胃松弛反应(迷走神经阻滞后胃内体积变化量 = 11 ± 5 ml,迷走神经复温后为194 ± 36 ml;P < 0.05)。双侧手术切断迷走神经也模拟了冷却引起的急性和可逆性迷走神经阻滞的这种效应。我们得出结论,一种非肾上腺素能、非胆碱能机制参与十二指肠扩张诱发的胃松弛。该机制由迷走神经介导。