肠衰竭的再认识

各种病因引起的肠衰竭均可导致肠消化吸收、运动或屏障免疫等功能障碍，随后营养缺乏、肠菌易位或内毒素血症，进而引发全身炎症反应综合征（systemicinflammatoryresponsesyndrome，SIRS）、     

肠黏膜功能障碍与肠衰竭

长期以来,人们对肠道功能的认识偏重于营养物的消化、吸收。通常所称的“肠衰竭”是指肠消化吸收功能因各种原因产生了障碍,包括短肠综合征、吸收不良综合征、慢性腹泻、假性肠梗阻及慢性炎症性肠病等。通常认为,危重症患者胃肠处于休眠状态。近年来,对肠道功能和肠衰竭的认识有了新的进展。肠道在消化吸收营养物质的同时,能维持肠道菌群稳定,防止肠道内细菌及内毒素移位,后者是导致全身炎症应答综合征（SIRS）、多器官功能障碍综合征（MODS）甚至多系统器官衰竭（MSOF）的一个重要因素。因此肠黏膜屏障功能已成为判断危重患者预后的一个重要指标。     

抗肠神经元抗体与胃肠道运动功能障碍性疾病研究进展

肠道神经系统对维持胃肠道功能发挥着极其重要的作用。近年来的研究显示,针对肠神经元的自身抗体可导致胃肠道运动功能的异常,可能是一些肠道动力相关疾病发生的重要机制。本文主要针对抗Hu抗体、抗钾离子通道抗体、钙离子通道抗体和抗尼古丁乙酰胆碱受体抗体等与胃肠道运动功能障碍性疾病关系的研究进展进行综述。     

重视肠屏障功能的研究

肠道除具有消化吸收食物及蠕动功能外，还有激素分泌、免疫调节和黏膜屏障功能。当肠功能紊乱，不能满足机体对营养物质及液体需求时，即为肠功能障碍。肠道屏障在维护肠功能中扮演着重要角色，它由机械屏障、化学屏障、微生物屏障和免疫屏障等组成。其中，机械屏障由肠道黏液层、肠黏膜上皮细胞、细胞间紧密连接等构成；化学屏障也称“肠-肝轴”，由胃肠道分泌的胃酸、胆汁、各种消化酶、溶菌酶、粘多糖等化学物质构成；微生物屏障则由肠道常驻菌群的微生态平衡构成；而免疫屏障主要由肠道免疫系统的细胞群构成。     

肠道细菌、肠黏膜屏障与肠功能障碍

肠黏膜屏障功能是胃肠道重要功能之一,黏膜屏障受损是肠功能障碍的重要原因,肠道细菌对于维护肠黏膜屏障功能十分重要,对于肠道细菌及肠黏膜屏障的重新认识将有利于临床工作的开展。     

肝功能衰竭患者的胃肠道手术

肝功能衰竭患者非肝脏手术后的发病和死亡风险较非肝功能衰竭患者增高。肝硬化患者急诊手术后死亡率高于择期手术后。对接受非肝脏手术的肝功能衰竭患者行术前评估极为重要，可降低高术后并发症和死亡风险。     

肝功能衰竭患者胃肠道屏障障碍及其治疗研究进展

肝衰竭是多种因素引起的严重肝损害,最终导致肝脏在合成、解毒、排泄和生物转化等方面的功能严重失常或失代偿,出现以凝血机制障碍和黄疸、肝性脑病、腹水等为主要表现的一组临床证候群[1］.肝功能衰竭会导致及加重肠道屏障功能障碍,而这种功能失常是推进肝功能衰竭向前进展的重要因素.现将近几年肝功能衰竭患者胃肠道屏障功能障碍的机制及治疗研究进展综述如下.     

胃肠道黏膜屏障与自身免疫性疾病

肠黏膜具有免疫和屏障功能。一方面，消化道黏膜不断地与病毒、细菌等微生物接触，在机体内担负起第一线的局部防御任务。另一方面，该系统对于食源性抗原、肠内常驻细菌可以产生免疫耐受。此种识别机制是由一个特殊的肠黏膜免疫组织“肠相关淋巴样组织”（gut associated lymphoidtissue，GALT）承担的。     

肠内营养与肠黏膜屏障的保护

肠黏膜屏障主要由机械屏障、生物屏障、化学屏障和免疫屏障肠黏膜屏障组成.根据肠屏障的结构、受损原因及病理生理过程的变化,可将肠屏障功能保护措施分为针对维持肠道微生态平衡及针对保护肠上皮细胞功能两大类.     

肠功能衰竭相关性肝病治疗策略

20世纪60年代后期,Douglas Wilmore和Stanley Dudrick在费城儿童医院成功地进行了一次肠外营养（PN）：一个小肠几乎完全闭锁的儿童通过PN存活下来,成长发育,并顺利转换为肠内营养。     

肠缺血时肠道细菌移居的实验研究

目的观察肠缺血时肠粘膜的病理改变及肠道细菌移居的时间特征。方法结扎大鼠回肠末段系膜动脉分支制作肠缺血模型，以缺血后２，６，１２ｈ测定门脉血及心脏血内毒素，取肠系膜淋巴结（ＭＬＮ）、肝、脾、血液作细菌培养，光镜及电镜观察缺血与缺血边缘区肠粘膜变化。结果缺血及缺血边缘区肠粘膜均受损；缺血早期门脉血对潘（３８９．０±１０５．０ｎｇ／Ｌ，ｖｓ５５．１±６．７ｎｇ／Ｌ，ｎ＝２０，ｔ＝１２ｈ，Ｐ＜０．０１）及心脏血内毒素（２４５．０±８８．０ｎｇ／Ｌ，ｖｓ４０．９±６．５ｎｇ／Ｌ，ｎ＝２０，ｔ＝１２ｈ，Ｐ＜０．０１），明显升高；ＭＬＮ、肝、脾、血液内都有肠道细菌存在。结论肠缺血使粘膜屏障受损，造成肠腔内细菌移居及内毒素入血，内毒素加重肠粘膜损害，形成恶性循环     

GLP-1在摄食和胃肠道生理功能中的作用

早期研究发现胰高血糖素样肽-1(GLP-1)作为一种肠道肽,具有葡萄糖依赖的胰岛素释放作用,后来在中枢神经系统中亦发现它的存在,消化道和脑中的GLP-1行使着多种生理功能,包括传递神经信号,调节摄食和饮水,调节体温和能量代谢,抑制胃肠分泌和运动,调节细胞的增殖和存活等.本文主要从GLP-1的合成与分泌,在脑中的分布,GLP-1对摄食和胃肠运动的影响,以及其临床应用潜力对它进行阐述.     

Cellular localization of a vasoactive intestinal peptide in the mammalian and avian gastrointestinal tract

Immunohistochemical studies using an antiserum to a pure porcine vasoactive intestinal peptide, possessing no cross reactivity against the related hormones glucagon, secretin, and gastrin-inhibitory peptide, revealed a wide distribution of vasoactive intestinal peptide cells throughout the entire length of the mammalian and avian gut. The highest numbers of cells were present in the small intestine and more particularly in the large intestine in all species investigated.Three types of endocrine cell in the mammalian gut are sufficiently widely distributed to be considered as the sites for production of vasoactive intestinal peptide. In the avian gut there are only two identifiable cell types.Sequential immunofluorescence and silver staining showed, in the bird, that the enterochromaffin (EC) cell was not responsible. This procedure could not be used in our mammalian gut samples but here serial section immunofluorescence for enteroglucagon and vasoactive intestinal peptide indicated that the two cells were not identical and that each was differently localized in the mucosa.These results leave the D cell of the Wiesbaden classification as the most likely site for the production of vasoactive intestinal peptide. The final identification must come from successful immune electron cytochemistry but this has not yet been achieved.     

Vasoactive intestinal polypeptide gene expression in the developing human gastrointestinal tract.

Expression of vasoactive intestinal polypeptide has been shown, by immunocytochemistry and biochemical assay, to follow the craniocaudal neural colonization of the mammalian gut. The aim of this study was to use in situ hybridization to see if it could provide more information on vasoactive intestinal polypeptide gene expression in the developing human gut. Immunocytochemistry of vasoactive intestinal polypeptide and, to visualize the total innervation, protein gene product 9.5 was also applied. By 8 weeks of gestation, protein gene product 9.5-immunoreactive neurons had colonized the gut lengthwise (17% of intestinal muscle area) but not transversely. Vasoactive intestinal polypeptide immunoreactivity was first detected at 9 weeks of gestation in a few nerve fibers of the upper gut, the origin of which could not be determined. Vasoactive intestinal polypeptide-immunoreactive ganglion cells were not seen until 18 weeks of gestation, whereas in situ hybridization showed messenger RNA in ganglion cells of the upper gut at 9 weeks. An adultlike pattern of peptide gene products (e.g., 2.5% and 3.1% of intestinal mucosal or muscle area, respectively) was detected by 20 weeks' gestation. The finding that the vasoactive intestinal polypeptide gene is expressed first in the upper human gut is consistent with craniocaudal neuronal colonization and maturation.