盐酸戊乙奎醚对小鼠血浆血管活性肠肽的影响

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目的观察盐酸戊乙奎醚对小鼠胃肠动力及血浆血管活性肠肽的影响。方法健康昆明小鼠30只,体重18~24g,雌雄不限,随机分为对照组、阿托品组和盐酸戊乙奎醚组,每组10只。阿托品组腹腔注射阿托品0.3mg/kg,盐酸戊乙奎醚组腹腔注射盐酸戊乙奎醚0.3mg/kg,对照组给予等容量0.9%氯化钠溶液。3组给药15min后以营养性半固体糊0.8ml/只灌胃,30min后处死小鼠,采用放免法测定血管活性肠肽水平,计算胃内残留率。结果与对照组比较,阿托品组血管活性肠肽水平升高(P<0.05),盐酸戊乙奎醚组血管活性肠肽水平差异无统计学意义(P>0.05);与阿托品组比较,盐酸戊乙奎醚组血管活性肠肽水平下降(P<0.05)。与对照组比较,阿托品组胃内残留率升高,盐酸戊乙奎醚组胃内残留率差异无统计学意义(P>0.05);与阿托品组比较,盐酸戊乙奎醚组胃内残留率降低(P<0.05)。结论与阿托品比较,盐酸戊乙奎醚不抑制胃肠运动,其对血管活性肠肽的分泌无影响。 Objective To observe the effects of penehyclidine hydrochloride on gastrointestinal motility and vasoactive intestinal peptide in mice. Methods Thirty healthy Kunming mice weighing 18-24 g were randomly divided into control group, atropine group and penehyclidine hydrochloride group, with 10 rats in each group. Atropine group intraperitoneal injection of atropine 0.3mg / kg, penehyclidine hydrochloride group intraperitoneal injection of penehyclidine hydrochloride 0.3mg / kg, the control group was given 0.9% sodium chloride solution. The rats in the three groups were administrated with nutritious semi-solid paste 0.8ml / g for 15min, and mice were sacrificed after 30min. The level of vasoactive intestinal peptide was determined by radioimmunoassay and the residual rate in the stomach was calculated. Results Compared with the control group, the levels of vasoactive intestinal peptide in the atropine group were significantly increased (P <0.05), and the levels of vasoactive intestinal peptide in the penehyclidine hydrochloride group were not significantly different (P> 0.05). Compared with the atropine group, The level of vasoactive intestinal peptide decreased in the test group (P <0.05). Compared with the control group, the gastric residual rate in the atropine group was increased, and there was no significant difference in the gastric residual rate in the penehyclidine hydrochloride group (P> 0.05). Compared with the atropine group, the residual gastric rate in the penehyclidine hydrochloride group Decreased (P <0.05). Conclusion Compared with atropine, penehyclidine hydrochloride did not inhibit gastrointestinal motility and had no effect on the secretion of vasoactive intestinal peptide.
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