Gallbladder contractility in aspirin- and cholesterol-fed prairie dogs.
Gallbladder contractility in aspirin- and cholesterol-fed prairie dogs.
复制标题
阿司匹林和胆固醇喂养的草原土拨鼠的胆囊收缩力。
DOI：
10.1016/0016-5085(94)90424-3
复制
发表时间：
1994
期刊：
影响因子：
29.4
通讯作者：
Moody,FG
中科院分区：
文献类型：
--
作者：
Li,YF;Russell,DH;Myers,SI;Weisbrodt,NW;Moody,FG
背景/目的：阿司匹林是否可以预防胆固醇胆结石的形成存在争议。本研究旨在调查这一问题，并确定与胆固醇喂养有关的草原土拨鼠胆囊平滑肌收缩力的抑制。方法：将草原土拨鼠分为四个亚组。动物喂食对照或 1.2% 胆固醇饮食，并用安慰剂或阿司匹林治疗 2 周。确定晶体和结石的存在，并测量胆囊肌肉条对胆囊收缩素八肽 (CCK-8) 的反应收缩力。 结果：在对照饮食的动物肌肉条中测量到的最大应力为 2.66 ± 0.23 × 104N/m2。高胆固醇饮食动物的最大应激显着降低，安慰剂组为 1.49 ± 0.16 × 104N/m2，阿司匹林组为 1.62 ± 0.23 × 104N/m2。阿司匹林治疗和安慰剂治疗动物之间的最大应激差异不显着。尽管对照组饮食的动物均未出现晶体或结石，但所有高胆固醇饮食的动物，无论接受安慰剂还是阿司匹林，其胆汁中均存在晶体，并且超过 65% 的动物患有胆固醇结石。 结论：阿司匹林对结石形成没有影响，也不能阻止收缩力的下降，尽管内源性胆囊前列腺素合成显着减少。
Background/Aims:Whether aspirin prevents cholesterol gallstone formation is controversial. This study aimed to investigate this issue and determine the depression of gallbladder smooth muscle contractility associated with cholesterol feeding in the prairie dog.Methods:Prairie dogs were divided into four subgroups. Animals were fed control or 1.2% cholesterol diet and treated with placebo or aspirin for 2 weeks. The presence of crystals and stones was determined, and contractile force in response to cholecystokinin octapeptide (CCK-8) of gallbladder muscle strips was measured.Results:Maximal stress of 2.66 ± 0.23 × 104N/m2was measured in muscle strips from animals on control diet. Maximal stress was significantly lower in strips from animals on high-cholesterol diet, being 1.49 ± 0.16 × 104N/m2with placebo and 1.62 ± 0.23 × 104N/m2with aspirin. The difference in maximal stress between aspirin-treated and placebo-treated animals was not significant. Although none of the animals on control diet had crystals or stones, all animals on the high-cholesterol diet, whether receiving placebo or aspirin, had crystals in the bile, and more than 65% had cholesterol stones.Conclusions:Aspirin has no effect on stone formation, nor does it prevent the decrease in contractility despite a profound decrease in endogenous gallbladder prostanoid synthesis.