早期肠内营养联合肠道去污对犬急性坏死性胰腺炎尿中甘露醇/乳果糖的影响

目的:观察早期肠内营养(EN)联合肠道去污(SDD)对犬急性坏死性胰腺炎(ANP) 肠黏膜结构、尿中的甘露醇/乳果糖的影响。方法:经腹向胰管内注入5%牛磺胆酸钠胰蛋白酶混合液(1 ml/kg)诱导ANP。20条杂种犬随机分为生理盐水(NS)组(n=5)、SDD组(n=5)、EN组(n=5)、SDD联合EN(ESDD)组(n=5)。在诱导ANP24 h后给予治疗,维持5 d。在治疗的第1、2、3、4、5天测定外周血的淀粉酶、乳酸脱氢酶。第2、5天测定尿中的甘露醇/乳果糖。实验第7天处死动物。分别取空肠、回肠、结肠测定绒毛高度、粘膜厚度。结果:①各组中淀粉酶、乳酸脱氢酶均无显著性差异。②EN和ESDD组小肠绒毛高度和肠粘膜厚度均高于SDD组和NS组(P<0.05)。③NS组第5天尿中的乳果糖/甘露醇明显高于EN、SDD组和ESDD组(P<0.05)。其中EN和SDD组第5天尿中的乳果糖/甘露醇明显高于ESDD组(P<0.05)。而第2 天尿中的乳果糖/甘露醇无明显差异。结论:EN、SDD和ES DD在犬急性坏死性胰腺炎中能够维持肠道粘膜的正常结构和功能,其中ESDD效果最佳。     

口饲乳果糖对失血性休克大鼠预后的影响

为了进一步阐明失血性休克预后与继发性内源性内毒素血症的直接关系，作者探讨了用口饲乳果糖清除肠道内毒素对大鼠失血性休克的保护作用。造成休克前，首先给大鼠口腔管饲２０％乳果糖（５ｍｌ／ｄ）或等容量生理盐水７天，每天给药２次。结果：休克后４８ｈ，乳果糖组大鼠存活率要明显高于盐水组（１０／１０与４／９，Ｐ＜０．０１）。休克后９０ｍｉｎ和１２０ｍｉｎ，乳果糖组大鼠血浆内毒素、ＴＮＦ水平均显著低于盐水组。提示：继发于失血性休克的内源性内毒素血症及肿瘤坏死因子在促使休克向不可逆性发展中可能起重要作用。作者认为，临床上对严重的失血性休克患者，除作复苏外，还应针对感染，尤其是内毒素血症尽早采取防护措施。     

The role of microbiota in hepatic encephalopathy

Hepatic encephalopathy (HE), which consists of minimal (MHE) and overt (OHE) stages, is a model for impaired gut-liver-brain axis in cirrhosis. Microbiota changes in both stages have been associated with impaired cognition, endotoxemia, and inflammation. There is dysbiosis (reduced autochthonous taxa [Lachnospiraceae, Ruminococcaceae, and Clostridiales XIV] and increased Enterobacteriaceae and Streptococcaceae) with disease progression. In MHE, there is an increased abundance of Streptococcus salivarius linked to cognition and ammonia. In OHE, stool Alcaligenaceae and Porphyromonadaceae are associated with poor cognition. Colonic mucosal microbiome in cirrhosis is significantly different compared with stool and independently related to cognition. HE treatment can affect microbial composition and function; cognitive improvement in MHE after rifaximin, a non-absorbable antibiotic, occurred without significant stool microbiota composition change but improved metabolic linkages. Similarly, there are only modest lactulose and rifaximin-associated changes on microbiota composition in OHE. HE represents an important model to study microbiome-brain interactions.     

Bovine colostrum supplementation during running training increases intestinal permeability

Endurance exercise training can increase intestinal permeability which may contribute to the development of gastrointestinal symptoms in some athletes. Bovine colostrum (BC) supplementation reduces intestinal permeability induced by non-steroidal anti-inflammatory drugs. This study aimed to determine whether BC could also reduce intestinal permeability induced by endurance exercise. Thirty healthy adult males (25.0 ± 4.7 yr; mean ± SD) completed eight weeks of running three times per week for 45 minutes at their lactate threshold while consuming 60 g/day of BC, whey protein (WP) or control (CON). Intestinal permeability was assessed at baseline and after eight weeks by measuring the ratio of urinary lactulose (L) and rhamnose (R) excretion. After eight weeks the L/R ratio increased significantly more in volunteers consuming BC (251 ± 140%) compared with WP (21 ± 35%, P < 0.05) and CON (-7 ± 13%, P < 0.02). The increase in intestinal permeability with BC may have been due to BC inducing greater leakiness of tight junctions between enterocytes or by increasing macromolecular transport as it does in neonatal gut. Further research should investigate the potential for BC to increase intestinal macromolecular transport in adults.     

Inhibition of secondary bile acid formation in the large intestine by lactulose in healthy subjects of two different age groups

Secondary bile acids have been implicated in colonic carcinogenesis. Transformation of primary into secondary bile acids (7 alpha-dehydroxylation) in the large bowel is a pH-dependent process. Inhibition of this reaction could be achieved by lowering colonic pH. We, therefore, studied the effects of lactulose (a non-absorbable disaccharide), which is capable of acidifying colonic contents, on secondary bile acid metabolism. Because this metabolism is age dependent, lactulose was given (0.3 g kg-1 twice daily for 12 weeks) to nine middle-aged (age 31-54 years; mean 45.7) and ten elderly subjects (age 56-81 years; mean 66.4). Twice before, and after 6 and 12 weeks' lactulose administration, biliary and faecal bile acids, whole gut transit time, faecal weight and dry weight, and faecal pH were recorded. The concentration of (iso)lithocholic and deoxycholic acid in faeces was higher in elderly subjects (P less than 0.05) but the excretion was comparable. After lactulose the concentration and excretion of the major secondary bile acids decreased. The primary bile acid fraction rose from 5% before, to more than 20% after, lactulose (P less than 0.05). Faecal weight increased and faecal dry weight decreased, resulting in a higher faecal water output during lactulose. Whole gut transit time did not change. The faecal pH dropped after 6 (P less than 0.05) and further after 12 weeks' lactulose (P less than 0.05). The percentage deoxycholic acid in bile was higher, and cholic acid lower, in elderly subjects (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sugar Intolerance: Origin and Mechanisms of Symptoms?

The origin and mechanisms of symptoms in sugar intolerance were studied in 8 healthy volunteers. For two test periods, volunteers swallowed a probe with perfused catheters and an infusion catheter which migrated into the colon. A meal containing 40 g lactulose or 40 g sucrose was ingested; the sucrose meal was followed by colonic infusion of 40 g lactulose in order to bypass the small intestine. Recordings of small intestinal and colonic motility were performed. Abdominal pain, bloating, borborygmi, and flatulence were similar during both periods. Both meals increased small intestinal and colonic motility. Only 37% of the symptoms coincided in time with colonic motor events. Symptoms were not related to a specific motor event and were not correlated with breath hydrogen excretion. In conclusion, symptoms of sugar intolerance originate from the colon. They are not related to specific phasic motor events or to breath hydrogen excretion.     

双歧三联活菌联合乳果糖治疗肝硬化肠源性内毒素血症的疗效观察

[目的]观察双歧三联活菌联合乳果糖治疗肝硬化肠源性内毒素血症的疗效。[方法]86例肝硬化患者随机分对照组(40例)和治疗组(32例)。2组均给予常规综合治疗,观察组在常规综合治疗基础上给予双歧三联活菌胶囊联合乳果糖口服治疗;2组疗程均为3周。比较2组治疗后肝功能、凝血功能、血清内毒素(ET)、血氨、肿瘤坏死因子-!(TNF-!)、白细胞介素-6(IL-6)水平变化。[结果]治疗后观察组白蛋白(ALB)、凝血酶原活动度(PTA)较对照组升高(P0.05),血清总胆红素(TBil)、ET、血氨、TNF-!、IL-6较对照组明显降低(P0.01);观察组总有效率为87.0%,优于对照组的67.5%(P0.05)。[结论]双歧三联活菌联合乳果糖能够降低肝硬化患者ET和血氨,通过下调促炎因子TNF-!和IL-6水平,以达到缓解肝脏炎症、改善肝功能和凝血功能的作用。     

Cisapride decreasing orocecal transit time in patients with nonalcoholic steatohepatitis

Introduction With the development of economy, there has been an increasing prevalence of nonalcoholic fatty liver disease (NAFLD)in China.[1] Along with viral liver disease and alcoholic liver disease, NAFLD has become one of the three primary liver diseases in the Chinese population. According to the Brunt criteria, nonalcoholic steatohepatitis (NASH) is defined when lobular inflammation or perisinusoidal fibrosis is present on histological examination.[2] Previously NASH was conside…