摘要：
Objective To explore the effect of biliary obstruction caused acute acalculous cholecystitis (AAC) on ultrastructure of gallbladder interstitial cells of Cajal (ICCs),and the possible mechanism of impaired contraction of gallbladder smooth muscle. Methods Total 60 healthy adult guinea pigs were in this study. The guinea pigs AAC model was induced by common bile duct ligation (BDL). The guinea pigs were divided into five groups equally,including sham control group (Sham),BDL for 12 hours (BDL-12),24 hours (BDL-24),48 hours (BDL-48) and 72 hours (BDL-72)groups. The gallbladder specimens were collected by the end of study. Gallbladder pathological changes were observed with HE staining under light microscope. Three muscle strips were collected of each gallbladder,fixed in constant temperature water bath with different concentration of eight peptide cholecystokinin agonist (CCK-8,1010 mmol/L,10-9 mmol/L,10-8 mmol/L,10-7 mmol/L and 10-6mmol/L),acetylcholine (Ach,10-8 mmol/L,107 mmol/L,10-6 mmol/L,10-5 mmol/L,10-4 mmol/L)and potassium chloride (KC1) (60 mmol/L). The contraction activity of gallbladder muscle strips was recorded by tonotransducer. The ultrastracture changes of gallbladder ICC in sham,BDL-12 and BDL-72 groups was examined by transmission electron microscopy. Results There was no obvious inflammation in Sham and BDL-12 groups. Compared with sham group,there were significant differences of biology score of gallbladder in BDL-48 and BDL-72 groups (P＜0. 05). After adding CCK-8,Ach and KC1,the contraction amplitude of gallbladder muscle increased in each group,and in dose-dependent manner. Compared with sham group,the effect value of each other groups decreased significantly (P＜0. 05). Compared with sham group,the morphology of ICC changed in BDL-12group,and more obvious in BDL-72 group. Conclusion Biliary obstruction can induce AAC. At the earlier stage of ACC,the impaired contraction of gallbladder smooth muscle present even without gallbladder inflammation occurrence. ICC may play an important role in impaired contraction.%目的 探讨胆道梗阻诱发急性非结石性胆囊炎(AAC)对胆囊Cajal间质细胞超微结构的影响,并初步探究胆囊平滑肌收缩障碍的可能机制.方法 健康成年豚鼠60只,胆总管结扎(BDL)方法构建豚鼠AAC模型.平均分为5组,即假手术对照组(Sham)、BDLl2h(BDL-12)、24h (BDL-24)、48h(BDL-48)以及72h(BDL-72)组.到实验时间后收集胆囊标本,HE染色后光学显微镜观察各组胆囊病理改变.每只胆囊取3条肌条(8 mm×3 mm),固定于恒温浴槽,分别给予不同浓度的八肽胆囊收缩素(CCK-8,1010 mmol/L、109 mmol/L、10-8 mmol/L、107 mmol/L和10-6mmol/L)、乙酰胆碱(Ach,108 mmol/L、107 mmol/L、106 mmol/L、105 mmol/L和10-4 mmol/L)以及KCI(60 mmmol/L),利用张力换能器记录胆囊平滑肌肌条的收缩活动.采用透射电镜检测Sham 组、BDL-12组和BDL-72组豚鼠胆囊Cajal问质细胞的形态学改变.结果 Sham组和BDL-12组未见明显炎性反应;与Sham组相比,BDL-48组及BDL-72组胆囊组织病理学评分差异有统计学意义(P＜0.05).加入CCK-8、Ach和KCI后,各组胆囊平滑肌收缩振幅均增加,且呈浓度依赖性;与Sham组相比,各组效应值均有下降,有统计学意义(P＜0.05).与Sham组相比,BDL-12组胆囊Cajal间质细胞形态发生改变,BDL-72组改变更为明显.结论 胆道梗阻可以诱发AAC.在AAC 早期胆囊炎症尚未发生时便可能有胆囊平滑肌的收缩障碍存在,而胆囊Cajal间质细胞可能是收缩障碍的一个重要中间环节.
