Baracat E C, Collares E F
Departamento de Pediatria, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Brasil.
Braz J Med Biol Res. 1997 Nov;30(11):1363-9. doi: 10.1590/s0100-879x1997001100017.
The gastric emptying of liquids was investigated in male Wistar rats (8 to 10 weeks old, 210-300 g) dehydrated by water deprivation. In this model of dehydration, weight loss, hematocrit and plasma density were significantly higher in the dehydrated animals than in the control groups after 48 and 72 h of water deprivation (P < 0.05). Three test meals (saline (N = 10), water (N = 10) and a WHO rehydrating solution containing in one liter 90 mEq sodium, 20 mEq potassium, 80 mEq chloride and 30 mEq citrate (N = 10)) were used to study gastric emptying following water deprivation for 24, 48 and 72 h. After 72 h, gastric emptying of the water (39.4% retention) and rehydrating solution (49.2% retention) test meals was significantly retarded compared to the corresponding control groups (P < 0.05, Mann-Whitney test). The 72-h period of deprivation was used to study the recovery from dehydration, and water was supplied for 60 or 120 min after 67 h of deprivation. Body weight loss, hematocrit and plasma density tended to return to normal when water was offered for 120 min. In the animals supplied with water for 60 min, there was a recovery in the gastric emptying of water while the gastric emptying of the rehydrating solution was still retarded (53.1% retention; P < 0.02, Kruskal-Wallis test). In the group supplied with water for 120 min, the gastric emptying of the rehydrating (51.7% retention) and gluco-saline (46.0% retention) solutions tended to be retarded (P = 0.04, Kruskal-Wallis test). In this model of dehydration caused by water deprivation, with little alteration in the body electrolyte content, gastric emptying of the rehydrating solution was retarded after rehydration with water. We conclude that the mechanisms whereby receptors in the duodenal mucosa can modify gastric motility are altered during dehydration caused by water deprivation.
在通过禁水造成脱水的雄性Wistar大鼠(8至10周龄,体重210 - 300克)中研究了液体的胃排空情况。在这种脱水模型中,禁水48小时和72小时后,脱水动物的体重减轻、血细胞比容和血浆密度显著高于对照组(P < 0.05)。使用三种试验餐(生理盐水(N = 10)、水(N = 10)和一种每升含90毫当量钠、20毫当量钾、80毫当量氯和30毫当量柠檬酸盐的世界卫生组织补液溶液(N = 10))来研究禁水24小时、48小时和72小时后的胃排空情况。72小时后,与相应对照组相比,水(潴留率39.4%)和补液溶液(潴留率49.2%)试验餐的胃排空明显延迟(P < 0.05,曼 - 惠特尼检验)。采用72小时的禁水期来研究脱水后的恢复情况,在禁水67小时后供水60分钟或120分钟。供水120分钟后,体重减轻、血细胞比容和血浆密度趋于恢复正常。在供水60分钟的动物中,水的胃排空有所恢复,而补液溶液的胃排空仍延迟(潴留率53.1%;P < 0.02,克鲁斯卡尔 - 沃利斯检验)。在供水120分钟的组中,补液溶液(潴留率51.7%)和葡萄糖盐水(潴留率46.0%)的胃排空趋于延迟(P = 0.04,克鲁斯卡尔 - 沃利斯检验)。在这种由禁水引起的脱水模型中,机体电解质含量变化不大,用水补液后补液溶液的胃排空延迟。我们得出结论,在由禁水引起的脱水过程中,十二指肠黏膜中的受体调节胃动力的机制发生了改变。