胆囊结石形成的动力学机制

目的 进一步探讨胆囊结石形成的动力学机制。方法 选用家兔57只,随机分为5组：（1）正常对照组（13只）,给予标准家兔饲料;（2）高胆固醇组（14只）,给予含1．2％胆固醇的高胆固醇饲料;（3）高胆固醇＋消炎痛组（10只）,给予高胆固醇饲料加消炎痛;（4）高胆固醇＋红霉素组（10只）,给予高胆固醇饲料加能促进胆囊收缩的红霉素;（5）高胆固醇＋动力散组（10只）,给予高胆固醇饲料加能促进胆囊收缩的动力散。结果 第1至第5组生成结石者分别为0只、12只、4只、0只及2只,第2组动物胆汁中胆固醇和粘蛋白浓度、胆囊管阻力、胆总管压力均较第1组显著增高（P＜0．01）,胆囊排空率下降（P＜0．01）;第3组胆汁粘蛋白浓度、胆囊管阻力、胆总管压力较第2组显著降低（P＜0．05）。第4组和第5组与第2组相比,胆汁中粘蛋白含量及胆囊管阻力低（P＜0．01）,胆囊排空率高（P＜0．05）。结论 除胆汁成分异常外,胆囊排空障碍是胆囊结石形成的关键因素。     

自制动力散预防胆囊结石形成的实验研究

为探讨中药动力散预防胆囊结石的机理，选用家兔３７只，随机分为３组。对照组（ｎ＝１３）给予基础饲料；高胆固醇组（ｎ＝１４）给予含１．２％胆固醇的高胆固醇饲料；高胆固醇＋动力散组（ｎ＝１０）给予高胆固醇饲 有促进胆囊收缩的中药动力散，分笼饲养４周后，对胆囊成平川 胆囊管阻力先进进行观察与检测。结果发现，高胆固醇组１２／１４只形成结石，高胆固醇＋动力散组２／１０只形成结石，后者动物胆囊排空率较高胆固率     

肝外胆道动力学因素对胆囊结石形成的影响

为了进一步明确胆道动力学因素对胆囊结石形成的影响，选用家兔２７只，随机分为两组，分别给予标准饲料和含１．２％胆固醇的高胆固醇饲料，４周后观察肝外胆道动力学变化，结果发现，高胆固醇组１２／１４形成结石，且该组动物除胆汁中胆固醇和粘蛋白浓度增高外，胆总管压力和胆囊管阻力均显著增高，外观胆囊体积增大，胆囊排空率显著降低，提示，除胆汁成分异常外，整个肝外胆道动力学因素参与了胆囊结石形成。     

消炎痛,红霉素预防胆囊结石形成的实验研究

为进一步探讨胆汁成份异常、胆囊动力学变化和胆囊结石形成之间的内在联系，对家兔胆囊结石动物模型进行了胆囊动力学研究。结果显示：除胆汁成份异常外，胆囊动力学变化参与了胆囊结石形成。消炎痛能减少胆汁粘蛋白含量抑制胆固醇成核过程而防止胆囊结石形成；而红霉素能通过促进胆囊收缩同时减少胆汁粘蛋白含量和促进胆囊排空，从而更有效地防止胆囊结石形成。提示：改善致石胆汁引起的胆囊动力学变化较改变胆汁成分更有利于防止胆囊结石形成。     

咖啡因预防家兔胆囊结石形成的研究

选用新西兰家兔18只,分三组,分别给予标准饲料、1.2％高胆固醇饲料及在高胆固醇料中加入咖啡因饲养8周。结果发现用高胆固醇饲料饲养的6只动物中有5只形成肥囊结石,而加用咖啡因的动物无一例形成结石,且该组胆囊胆汁与肝胆汁的胆酸比值及钠比值均显著降低。实验表明咖啡因可通过抑制胆囊吸收功能、增加肝胆汁流量、降低胆汁粘蛋白浓度,有效地防止胆囊胆固醇结石形成。     

胆囊运动在胆固醇结石形成中的作用（综述）

胆囊运动的异常与胆囊结石的形成紧密相关。胆囊伴发结石时，可有胆囊收缩改变和排空减少。在胆固醇结石的病例，胆囊收缩减弱更与胆汁成石指数相关。在胆囊结石形成过程中，胆囊收缩异常与胆法成份改变互相影响，促进结石形成。     

胆囊运动在胆固醇结石形成中的作用

胆囊运动的异常与胆囊结石的形成紧密相关.胆囊伴发结石时,可有胆囊收缩改变和排空减少、在胆固醇结石的病例,胆囊收缩减弱更与胆汁成石指数相关.在胆囊结石形成过程中,胆囊收缩异常与胆汁成份改变互相影响,促进结石形成.     

胆囊动力学变化对胆囊结石形成的作用

目的 探讨胆囊动力学变化对胆囊结石形成的作用.方法 收集2007年8月至12月武警安徽省总队医院行LC患者的临床资料.根据胆囊结石中胆固醇的含量,将39例胆囊结石患者分为胆色素结石组(13例)、胆固醇结石组(13例)和混合性结石组(13例),分别检测胆囊收缩功能,胆囊壁缩胆囊素受体含量及活性,并将胆囊无结石、炎症的正常者设为对照组(13例).结果 (1)胆囊排空率、胆囊壁缩胆囊索受体含量及活性:胆色素结石组>混合性结石组>胆固醇结石组.(2)胆囊壁缩胆囊素受体含量及活性与胆囊排空率呈正相关(r=0.969,0.938,P<0.01);与结石中胆固醇含量呈负相关(r=-0.949,-0.979,-0.987,P<0.01).结论 胆囊结石中胆固醇含量与胆囊动力、缩胆囊素受体关系密切,可能是胆固醇通过影响缩胆囊素而降低了胆囊动力,促进了胆固醇结石的形成.     

胆囊动力学变化对胆囊结石形成的作用

目的 探讨胆囊动力学变化对胆囊结石形成的作用.方法 收集2007年8月至12月武警安徽省总队医院行LC患者的临床资料.根据胆囊结石中胆固醇的含量,将39例胆囊结石患者分为胆色素结石组(13例)、胆固醇结石组(13例)和混合性结石组(13例),分别检测胆囊收缩功能,胆囊壁缩胆囊素受体含量及活性,并将胆囊无结石、炎症的正常者设为对照组(13例).结果 (1)胆囊排空率、胆囊壁缩胆囊索受体含量及活性:胆色素结石组>混合性结石组>胆固醇结石组.(2)胆囊壁缩胆囊素受体含量及活性与胆囊排空率呈正相关(r=0.969,0.938,P<0.01);与结石中胆固醇含量呈负相关(r=-0.949,-0.979,-0.987,P<0.01).结论 胆囊结石中胆固醇含量与胆囊动力、缩胆囊素受体关系密切,可能是胆固醇通过影响缩胆囊素而降低了胆囊动力,促进了胆固醇结石的形成.     

胆囊动力学变化对胆囊结石形成的作用

目的 探讨胆囊动力学变化对胆囊结石形成的作用.方法 收集2007年8月至12月武警安徽省总队医院行LC患者的临床资料.根据胆囊结石中胆固醇的含量,将39例胆囊结石患者分为胆色素结石组(13例)、胆固醇结石组(13例)和混合性结石组(13例),分别检测胆囊收缩功能,胆囊壁缩胆囊素受体含量及活性,并将胆囊无结石、炎症的正常者设为对照组(13例).结果 (1)胆囊排空率、胆囊壁缩胆囊索受体含量及活性:胆色素结石组>混合性结石组>胆固醇结石组.(2)胆囊壁缩胆囊素受体含量及活性与胆囊排空率呈正相关(r=0.969,0.938,P<0.01);与结石中胆固醇含量呈负相关(r=-0.949,-0.979,-0.987,P<0.01).结论 胆囊结石中胆固醇含量与胆囊动力、缩胆囊素受体关系密切,可能是胆固醇通过影响缩胆囊素而降低了胆囊动力,促进了胆固醇结石的形成.     

Stasis before gallstone formation: Altered gallbladder compliance or cystic duct resistance?

Gallbladder stasis occurs before gallstone formation and provides the link between the hepatic secretion of supersaturated bile and cholesterol cholelithiasis. We recently observed that cystic duct resistance increases while sphincter of Oddi resistance is unchanged in the presence of lithogenic bile without gallstones. Whether alterations in gallbladder function also lead to gallbladder stasis has been unclear. Therefore, we tested the hypothesis that before gallstone formation, stasis results from increased cystic duct resistance and altered gallbladder compliance. Adult, male prairie dogs were fed either a trace cholesterol (control) or a 0.4 percent cholesterol-enriched diet. Cystic duct resistance increased but gallbladder compliance was unchanged before gallstone formation. A significant correlation (p < 0.001) was found between the lithogenic index and cystic duct resistance in pregallstone animals. We conclude that increased resistance to flow across the cystic duct, and not altered gallbladder compliance, is etiologically related to bile stasis, an important event in gallstone formation.     

The role of cystic duct resistance in the pathogenesis of cholesterol gallstones

Several recent clinical and laboratory observations suggest that impaired gallbladder emptying is important in the pathogenesis of cholesterol cholelithiasis. However, the exact mechanism by which gallbladder stasis occurs in the majority of patients who form gallstones has not been clear. We tested the hypothesis that impaired gallbladder emptying antedates cholelithiasis and results from increased resistance to bile flow. Using the prairie dog gallstone model, resistance to flow through the cystic duct (CD) and sphincter of Oddi (SO) was measured in control and cholesterol-fed animals. Prairie dogs were fed either a control (trace cholesterol) or a 0.4% cholesterol-enriched diet known to induce gallstones in 6 weeks. Resistance across the CD and SO was measured at 4 weeks (pregallstone) and 16 weeks (gallstone). Resistance was measured by infusing lactated Ringer's solution through the CD and SO at four separate flow rates while gallbladder and distal common bile duct pressures were recorded. Resistance to flow through the cystic duct increased prior to gallstone formation and continued to increase during the 16 weeks of cholesterol feeding. In comparison, sphincter of Oddi resistance remained normal despite chronic exposure to lithogenic bile and formation of stones within the gallbladder. The increased cystic duct resistance observed prior to gallstone formation provides a mechanism for diminished gallbladder emptying and suggests an etiological role for increased cystic duct resistance in the pathogenesis of cholesterol gallstones.     

Role of gallbladder mucus in the pathogenesis of cholesterol gallstones

Recent observations indicate that the hepatic secretion of lithogenic bile, gallbladder mucus hypersection, and gallbladder stasis are all critical factors in the pathogenesis of cholesterol gallstones. Using the prairie dog gallstone model, we investigated the interaction of these factors and the sequence in which they develop. The results of this study indicated that (1) gallbladder bile mucus concentration is elevated before cholesterol precipitation and increases progressively with the formation of cholesterol crystals, (2) cystic duct resistance increases in the presence of cholesterol crystals, but not fine, sonicated crystals increase cystic duct resistance. We conclude that these alterations trigger a self-perpetuating cycle of mucus hypersecretion, cholesterol crystallization, and gallbladder stasis which culminates in the formation of cholesterol gallstones.     

Bile acid pattern of gallbladder and hepatic bile in patients with and without cholesterol gallstones.

Bile acid composition of hepatic and gallbladder bile was examined in a group of 18 patients with uncomplicated cholelithiasis and a control group consisting of 13 patients with healed duodenal ulcers. Bile specimens were taken during laparotomy. Molar concentrations of the different bile acids in hepatic and gallbladder bile were determined. The ratios between the molar concentrations of the different bile acids were calculated. In order to compare these molar ratios in hepatic and gallbladder bile the quotients between identical molar ratios of hepatic and gallbladder bile were calculated in each subject. Bile acid concentration of the gallbladder bile was found to be lower in the gallstone patients. Trihydroxy or dihydroxy bile acid molar ratio was lower in the gallstone group. Hepatic to gallbladder relative trihydroxy to dihydroxy and cholate to deoxycholate bile acid ratios were elevated in the gallstone patients. This might indicate that an increased formation of deoxycholate is the main cause for the decreased trihydroxy to dihydroxy bile acid molar ratio observed in the gallbladder bile of patients with cholesterol gallstones.     

胆、肠菌群差异性与胆囊胆固醇结石形成关系

目的 基于胆囊胆固醇结石患者胆道菌群、肠道菌群差异性,探讨胆、肠菌群交互与胆囊胆固醇结石形成关系.方法 选择2020年1月至2020年6月由沧州市人民医院诊疗的胆囊胆固醇结石患者42例为研究对象,记入胆固醇结石组;胆囊炎、胆囊息肉诊治等非胆固醇结石患者40例为非胆固醇结石组.采用Illumina测序技术测序并进行细菌O...     

The pathophysiological characteristics of bile from patients with gallstones: the role of prostaglandins and mucin in gallstone formation

Bile was obtained from 82 patients with various biliary tract diseases and concentrations of prostagloandins, leukotriens, mucin, and a number of lithogenic components were measured in order to evaluate the role of these substances in the pathogenesis of gallstone formation. The characteristics of bile in cases of cholesterol gallstones included high concentrations of prostaglandins and hexosamine and a high cholesterol saturation index. Prostaglandin E2 and prostaglandin F2 alpha concentrations in bile were correlated with hexosamine concentration, and prostaglandins and hexosamine were found to be actively synthesized and secreted in the gallbladder. Prostaglandins E2 and F2 alpha may therefore stimulate mucin secretion in the gallbladder with supersaturated bile. The characteristics of bile in cases of calcium bilirubinate gallstones included a high detection rate for bacteria, high beta-glucuronidase activity, a high percentage of unconjugated bilirubin, a low cholesterol saturation index and high concentrations of prostaglandins and hexosamine. Moreover, the synthesis and secretion of prostaglandins in the biliary tract were accelerated in cases of infected bile. Thus, hypersecretion of mucin, stimulated by prostaglandins, my participate in the onset and development of biliary tract infection or in the formation of calcium bilirubinate gallstones. Regarding the role of prostaglandins and mucin, the hypotheses for gallstone formation previously reported by many authors are supported by the clinical data obtained in the current study.     

An experimental study on preventing gallstone formation by exogenous cholecystokinin

It is well known that stasis of lithogenic bile in the gallbladder is an important factor in cholesterol gallstone formation. In this study, hamsters fed with standard lithogenic diet were given physiologic dose of exogenous cholecystokinin-octapeptide daily to facilitate emptying of the gallbladder. It was found that there was significant reduction in the gallstone formation. This study suggests that gallbladder motility is closely correlated with cholesterol gallstone formation, and administration of exogenous cholecystokinin-octapeptide can effectively prevent gallbladder stasis and reduce the incidence of cholelithiasis. This method may be useful for gallstone prophylaxis in high-risk individuals.     

瘦素对血脂及胆汁成分的调节在胆囊胆固醇结石形成中的作用

目的:分析胆囊胆固醇结石患者瘦素与血脂及胆囊内胆汁成分的关系,探讨瘦素在胆囊胆固醇结石形成中的作用。方法:选择胆囊胆固醇结石接受腹腔镜胆囊切除术的患者30例(结石组)与同期因胆囊息肉行腹腔镜胆囊切除术的患者22例(息肉组),检测患者血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、瘦素、胆囊胆汁中的TC与总胆汁酸(TBA)水平,以及胆囊壁组织瘦素受体mRNA水平。结果:与息肉组比较,结石组血清TC、TG、LDL、瘦素水平以及胆囊内胆汁TC/TBA含量比率与胆囊组织瘦素受体mRNA水平均明显升高,而血清HDL明显降低(均P0.05)。结石组的血清瘦素水平与血清TG、TC及胆汁TC均呈正相关(r=0.633,P=0.002;r=0.224,P=0.025;r=0.384,P=0.000),与HDL和TBA呈负相关(r=-0.205,P=0.014;r=-0.548,P=0.024)呈负相关,而息肉组血清瘦素与以上指标间均无关(均P0.05)。结论:瘦素参与了胆囊胆固醇结石的形成,瘦素及其受体水平的升高可能与胆囊胆固醇结石患者胆固醇代谢异常、胆囊胆汁成分失调密切相关。     

Effect of bile diversion and sphincterotomy on gallbladder muscle contractility and gallstone formation

Feeding prairie dogs a diet rich in cholesterol induces gallstone formation that is preceded by a sustained decrease in gallbladder smooth muscle contractility. Sphincterotomy is known to prevent gallstone formation in cholesterol-fed prairie dogs. Experiments were designed to determine whether the effect of sphincterotomy is a consequence of hepatic bile diversion, and whether bile diversion prevents the altered contractility. Following sham operation, surgical biliary enteric bypass, or sphincterotomy, prairie dogs were fed a high-cholesterol or a regular diet. Gallbladder muscle contractility and the presence of crystals and stones were determined. In sham-operated animals, the cholesterol diet induced a decrease in gallbladder muscle contractility and caused the formation of cholesterol gallstones. In animals with bile diversion and sphincterotomy, the effects of cholesterol feeding were reduced or prevented. Thus, these procedures may prevent stone formation by preventing a reduction in gallbladder contractility. Contractility was depressed in animals with bile diversion fed a regular diet, compared with animals with a sham operation fed a regular diet. The mechanism for this depression may differ from that induced by the cholesterol diet. Diversion, and perhaps sphincterotomy, impairs gallbladder filling. Thus, gallbladder muscle is not stretched and does not contract against a load. This could result in a "disuse atrophy." If the results from our study apply to humans, sphincterotomy may reduce stone formation by preventing the effects of lithogenic bile on gallbladder muscle contractility and by enhancing the ability of the muscle to empty the lithogenic bile.     

Transport of fluid and biliary lipids in the canine gallbladder in experimental cholecystitis

In acute cholecystitis the cystic duct is usually obstructed by a gallstone and the gallbladder is often tensely distended with clear fluid. Because these findings suggest that fluid absorption in the gallbladder may be reversed in cholecystitis, we examined the effect of inflammation on the gallbladder mucosal function in dogs. In 20 dogs cholecystitis was induced by ligating the cystic duct and allowing inflammation to develop from bile stasis and the presence of a chronic indwelling cannula in the gallbladder. Every morning an aliquot of normal hepatic bile was infused into the gallbladder through a cannula in the gallbladder fundus. After either 4 or 24 hr the gallbladder contents were aspirated, the volume was measured, and the concentrations of bile acids, cholesterol, phospholipids, and protein were determined. Changes in volume were checked using [14C]PEG as a nonabsorbable tracer. A net absorption of fluid, bile acids, cholesterol, and phospholipids occurred during the first 24 to 48 hr after ligation of the cystic duct. Thereafter, fluid, cholesterol, and protein were secreted into the lumen, but absorption of bile acids continued. The lithogenic index of bile placed in the inflamed gallbladder was always greater when the bile was removed 24 hr later. The rate of fluid secretion into the lumen of the inflamed gallbladder increased after a meal and decreased after indomethacin. These findings demonstrate that inflammation can stimulate the gallbladder mucosa to secrete fluid, a process that may be important in the pathophysiology of acute cholecystitis in man. Since inflammation also resulted in an increased cholesterol saturation of gallbladder bile, cholecystitis per se may contribute to the formation of cholesterol gallstones.