中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2011年
6期
396-400
,共5页
李湘楚%肖勇%余保平%赵梦%罗和生
李湘楚%肖勇%餘保平%趙夢%囉和生
리상초%초용%여보평%조몽%라화생
无结石性胆囊炎%间质细胞%胆囊排空%显微镜检查,电子%胆总管%结扎术%疾病模型,动物
無結石性膽囊炎%間質細胞%膽囊排空%顯微鏡檢查,電子%膽總管%結扎術%疾病模型,動物
무결석성담낭염%간질세포%담낭배공%현미경검사,전자%담총관%결찰술%질병모형,동물
Acalculous cholecystitis%Stromal cells%Gallbldder emptying%Microscopy,election%Common bile duct%Ligation%Disease moldels,animal
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.
目的 探討膽道梗阻誘髮急性非結石性膽囊炎(AAC)對膽囊Cajal間質細胞超微結構的影響,併初步探究膽囊平滑肌收縮障礙的可能機製.方法 健康成年豚鼠60隻,膽總管結扎(BDL)方法構建豚鼠AAC模型.平均分為5組,即假手術對照組(Sham)、BDLl2h(BDL-12)、24h (BDL-24)、48h(BDL-48)以及72h(BDL-72)組.到實驗時間後收集膽囊標本,HE染色後光學顯微鏡觀察各組膽囊病理改變.每隻膽囊取3條肌條(8 mm×3 mm),固定于恆溫浴槽,分彆給予不同濃度的八肽膽囊收縮素(CCK-8,1010 mmol/L、109 mmol/L、10-8 mmol/L、107 mmol/L和10-6mmol/L)、乙酰膽堿(Ach,108 mmol/L、107 mmol/L、106 mmol/L、105 mmol/L和10-4 mmol/L)以及KCI(60 mmmol/L),利用張力換能器記錄膽囊平滑肌肌條的收縮活動.採用透射電鏡檢測Sham 組、BDL-12組和BDL-72組豚鼠膽囊Cajal問質細胞的形態學改變.結果 Sham組和BDL-12組未見明顯炎性反應;與Sham組相比,BDL-48組及BDL-72組膽囊組織病理學評分差異有統計學意義(P＜0.05).加入CCK-8、Ach和KCI後,各組膽囊平滑肌收縮振幅均增加,且呈濃度依賴性;與Sham組相比,各組效應值均有下降,有統計學意義(P＜0.05).與Sham組相比,BDL-12組膽囊Cajal間質細胞形態髮生改變,BDL-72組改變更為明顯.結論 膽道梗阻可以誘髮AAC.在AAC 早期膽囊炎癥尚未髮生時便可能有膽囊平滑肌的收縮障礙存在,而膽囊Cajal間質細胞可能是收縮障礙的一箇重要中間環節.
목적 탐토담도경조유발급성비결석성담낭염(AAC)대담낭Cajal간질세포초미결구적영향,병초보탐구담낭평활기수축장애적가능궤제.방법 건강성년돈서60지,담총관결찰(BDL)방법구건돈서AAC모형.평균분위5조,즉가수술대조조(Sham)、BDLl2h(BDL-12)、24h (BDL-24)、48h(BDL-48)이급72h(BDL-72)조.도실험시간후수집담낭표본,HE염색후광학현미경관찰각조담낭병리개변.매지담낭취3조기조(8 mm×3 mm),고정우항온욕조,분별급여불동농도적팔태담낭수축소(CCK-8,1010 mmol/L、109 mmol/L、10-8 mmol/L、107 mmol/L화10-6mmol/L)、을선담감(Ach,108 mmol/L、107 mmol/L、106 mmol/L、105 mmol/L화10-4 mmol/L)이급KCI(60 mmmol/L),이용장력환능기기록담낭평활기기조적수축활동.채용투사전경검측Sham 조、BDL-12조화BDL-72조돈서담낭Cajal문질세포적형태학개변.결과 Sham조화BDL-12조미견명현염성반응;여Sham조상비,BDL-48조급BDL-72조담낭조직병이학평분차이유통계학의의(P＜0.05).가입CCK-8、Ach화KCI후,각조담낭평활기수축진폭균증가,차정농도의뢰성;여Sham조상비,각조효응치균유하강,유통계학의의(P＜0.05).여Sham조상비,BDL-12조담낭Cajal간질세포형태발생개변,BDL-72조개변경위명현.결론 담도경조가이유발AAC.재AAC 조기담낭염증상미발생시편가능유담낭평활기적수축장애존재,이담낭Cajal간질세포가능시수축장애적일개중요중간배절.
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.
