Narducci F, Bassotti G, Granata M T, Gaburri M, Farroni F, Palumbo R, Morelli A
Arch Intern Med. 1986 Apr;146(4):716-20.
Chronic idiopathic gastric stasis can be responsible for unexplained dyspepsia. Because exogenous opiates inhibit gastric emptying and endogenouslike substances are present in the gastrointestinal tract, we tested the hypothesis that increased endogenous opiate activity may be responsible for chronic idiopathic gastric stasis. Eighteen patients with chronic idiopathic gastric stasis and ten healthy volunteers were studied by gastrointestinal manometry. Scintigraphic technique also was used, during which either intravenous saline or naloxone hydrochloride were infused. Manometry showed gastric hypomotility in ten patients and duodenal hyperdyskinesia in the remaining eight patients. Naloxone did not alter gastric emptying in healthy subjects or corrected gastric stasis in patients with gastric hypomotility, while it normalized gastric emptying in patients with duodenal dyskinesia. It seems that either gastroparesis or duodenal dyskinesia can promote gastric stasis and chronic dyspepsia, and endogenous opiates participate in the pathogenesis of gastric stasis in patients with duodenal dyskinesia.
慢性特发性胃潴留可能是不明原因消化不良的病因。由于外源性阿片类药物会抑制胃排空，且胃肠道中存在内源性类似物质，我们检验了内源性阿片类活性增加可能是慢性特发性胃潴留病因的假说。通过胃肠测压法对18例慢性特发性胃潴留患者和10名健康志愿者进行了研究。还采用了闪烁扫描技术，期间输注静脉生理盐水或盐酸纳洛酮。测压显示，10例患者存在胃动力不足，其余8例患者存在十二指肠运动亢进。纳洛酮并未改变健康受试者的胃排空，也未纠正胃动力不足患者的胃潴留，而它使十二指肠运动障碍患者的胃排空恢复正常。似乎胃轻瘫或十二指肠运动障碍均可导致胃潴留和慢性消化不良，内源性阿片类物质参与十二指肠运动障碍患者胃潴留的发病机制。
