Armbrecht U, Dotevall G, Stockbrügger R W
Z Gastroenterol. 1987 Mar;25(3):145-50.
Orocoecal transit time was studied by means of a hydrogen (H2) breath test after a standard meal in patients with peptic disease before and during treatment with ranitidine, in patients with gastric achlorhydria, and in healthy acid-secreting volunteers. Treatment with ranitidine prolonged the orocoecal transit time in patients with peptic disease from 201.9 +/- 18.3 (SEM) to 242.3 +/- 18.3 min (p less than 0.05). Also in patients with achlorhydria, the orocoecal transit time was prolonged (276.2 +/- 20.3 min), compared to the control group of healthy acid-secreting volunteers (213.5 +/- 15.7 min), (p less than 0.05). The orocoecal transit time did not correlate with gastric bacterial concentrations in the groups investigated, nor with the subjects' age. It was not correlated to the pH in the gastric juice of acid-secreting individuals, either with or without treatment. As gastric emptying was not evaluated in this study, it is impossible to state whether gastric stasis or inhibited small bowel motility, or both, cause the delayed transit in achlorhydria and during treatment with ranitidine. We suggest that the reduction of gastric juice volume could be the cause.
在消化性疾病患者服用雷尼替丁治疗前及治疗期间、胃酸缺乏患者以及健康胃酸分泌志愿者中,通过标准餐后氢(H₂)呼气试验研究了口盲肠转运时间。雷尼替丁治疗使消化性疾病患者的口盲肠转运时间从201.9±18.3(标准误)分钟延长至242.3±18.3分钟(p<0.05)。与健康胃酸分泌志愿者对照组(213.5±15.7分钟)相比,胃酸缺乏患者的口盲肠转运时间也延长了(276.2±20.3分钟)(p<0.05)。在所研究的组中,口盲肠转运时间与胃细菌浓度以及受试者年龄均无相关性。无论是否接受治疗,其与胃酸分泌个体胃液中的pH值也不相关。由于本研究未评估胃排空情况,因此无法确定胃酸缺乏患者及雷尼替丁治疗期间的转运延迟是由胃潴留还是小肠运动抑制或两者共同引起的。我们认为胃液量减少可能是原因所在。