Parkman H P, Trate D M, Knight L C, Brown K L, Maurer A H, Fisher R S
Gastroenterology Section, Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania, USA.
Gut. 1999 Sep;45(3):346-54. doi: 10.1136/gut.45.3.346.
Cholinergic regulation of chronotropic (frequency) and inotropic (force) aspects of antral contractility and how these impact on gastric emptying are not well delineated.
To determine the effects of cholinergic stimulation and inhibition on myoelectric, contractile, and emptying parameters of gastric motility.
Ten normal subjects underwent three studies each, using simultaneous electrogastrography (EGG), antroduodenal manometry, and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of baseline fasting manometry and EGG, subjects received saline intravenously, atropine (0.6 mg then 0.25 mg/hour intravenously), or bethanechol (5 mg subcutaneously). This was followed by another 30 minutes' recording and by three hours of postprandial recording after ingestion of a technetium-99m labelled solid meal.
During fasting, atropine decreased, whereas bethanechol increased, the antral manometric motility index and EGG power. Postprandially, atropine decreased the amplitude of antral contractions by DAS, decreased the postprandial antral manometric motility index, and slowed gastric emptying. Atropine caused a slight increase in postprandial frequency of antral contractions by DAS and gastric myoelectrical activity by EGG. Bethanechol slightly increased the amplitude, but slightly decreased the frequency of antral contractions by DAS and decreased the frequency of gastric myoelectrical activity by EGG, with no significant increase in the motility index or gastric emptying.
Cholinergic antagonism with atropine reduces antral contractility and slows gastric emptying. Cholinergic stimulation with bethanechol increases antral contractility, but decreases the frequency of antral contractions, without altering the antral motility index or gastric emptying.
胆碱能对胃窦收缩性变时(频率)和变力(力量)方面的调节以及这些调节如何影响胃排空尚未得到很好的描述。
确定胆碱能刺激和抑制对胃动力的肌电、收缩和排空参数的影响。
10名正常受试者每人进行三项研究,同时使用胃电图(EGG)、十二指肠测压法以及动态胃窦闪烁扫描法(DAS)测量胃排空。在禁食状态下进行30分钟的基线测压和EGG检查后,受试者静脉注射生理盐水、阿托品(0.6毫克,然后以0.25毫克/小时静脉注射)或氨甲酰甲胆碱(5毫克皮下注射)。随后再进行30分钟的记录,并在摄入99m锝标记的固体餐食后进行三小时的餐后记录。
禁食期间,阿托品降低,而氨甲酰甲胆碱增加胃窦测压运动指数和EGG功率。餐后,阿托品通过DAS降低胃窦收缩幅度,降低餐后胃窦测压运动指数,并减缓胃排空。阿托品使餐后胃窦收缩频率通过DAS略有增加,使胃肌电活动通过EGG略有增加。氨甲酰甲胆碱使收缩幅度略有增加,但使胃窦收缩频率通过DAS略有降低,并使胃肌电活动频率通过EGG降低,胃动力指数和胃排空无显著增加。
阿托品的胆碱能拮抗作用降低胃窦收缩性并减缓胃排空。氨甲酰甲胆碱的胆碱能刺激增加胃窦收缩性,但降低胃窦收缩频率,而不改变胃窦动力指数或胃排空。