Dubois A, Gross H A, Richter J E, Ebert M H
Dig Dis Sci. 1981 Jul;26(7):598-600. doi: 10.1007/BF01367671.
We have shown previously that patients with primary anorexia nervosa (PAN) have decreased gastric emptying and acid output. The present studies were designed to explore the possibility that bethanechol, a parasympathomimetic agent, would acutely restore normal gastric function in those patients. We used a dye dilution technique to determine acid output and fractional emptying rate in 5 patients with PAN and 11 healthy controls during a basal period and following bethanechol (0.06 mg/kg, subcutaneously). Although bethanechol caused fractional emptying and acid output to increase threefold in PAN (P less than 0.05), it failed to produce stimulation of gastric emptying and acid output to levels similar to those achieved in controls. Therefore, gastric emptying and acid output were less in PAN than in controls, both basally and after bethanechol. Since bethanechol failed to completely restore acute gastric function, the defect of emptying and acid output in PAN does not appear to be caused by a deficiency of parasympathetic neurotransmitter but, instead, could reflect undetermined inhibitory influences or impaired function of the muscular and glandular cells. Following weight gain, fractional emptying rate and acid output were still slightly less in PAN patients than in controls, but the difference was statistically significant only for basal acid output.
我们之前已经表明,原发性神经性厌食症(PAN)患者的胃排空和胃酸分泌减少。本研究旨在探讨拟副交感神经药氨甲酰甲胆碱能否使这些患者的胃功能迅速恢复正常。我们采用染料稀释技术,在基础期及注射氨甲酰甲胆碱(0.06mg/kg,皮下注射)后,测定了5例PAN患者和11例健康对照者的胃酸分泌及胃排空分数率。尽管氨甲酰甲胆碱使PAN患者的胃排空分数率和胃酸分泌增加了两倍(P<0.05),但它未能将胃排空和胃酸分泌刺激到与对照组相似的水平。因此,无论是在基础期还是注射氨甲酰甲胆碱后,PAN患者的胃排空和胃酸分泌均低于对照组。由于氨甲酰甲胆碱未能完全恢复急性胃功能,PAN患者胃排空和胃酸分泌的缺陷似乎并非由副交感神经递质缺乏所致,而是可能反映了尚未明确的抑制性影响或肌肉和腺细胞功能受损。体重增加后,PAN患者的胃排空分数率和胃酸分泌仍略低于对照组,但仅基础胃酸分泌的差异具有统计学意义。