肠缺血后处理对兔缺血再灌注损伤小肠上皮细胞线粒体形态和功能的影响

目的观察缺血后处理对小肠缺血再灌注损伤的保护作用。方法30只大白兔随机分为3组，每组8只：A组，假手术组；B组，肠缺血再灌注损伤模型组；C组，肠缺血再灌注损伤模型肠缺血后处理组，实验结束后取小肠标本进行小肠上皮细胞形态和呼吸功能指标测定。结果A、C两组线粒体的数目、周长均大于B组，A、C两组问比较，A组较大（P〈0．05）。A、C两组线粒体的面积、最大直径、最小直径、等效直径均小于B组（P〈0．05），A、C两组间比较差异无统计学意义（P〉0．05）。B组线粒体的体积密度小于A组，面积密度、比表面和粒子数密度均小于其余两组（P〈0．05）。A、C两组间三维平面形态计量学各参数比较差异无统计学意义（P〉0．05）；B、C组线粒体呼吸控制比率（RCR）低于A组差异有统计学意义（P〈0．05），与C组比较，B组下降更为明显（P〈0．05）。结论小肠缺血后处理对缺血再灌注损伤肠上皮细胞线粒体形态和功能均有保护作用。     

亲属活体部分小肠移植术后早期并发症的防治

目的探讨亲属活体部分小肠移植术后早期并发症的防治。方法为3例短肠综合征患者和1例肠神经节缺失导致小肠无功能患者施行亲属活体部分小肠移植术,供、受者HLA配型均有4个以上抗原相合,供肠均取自回肠末端,长度为(150±10)cm,应用他克莫司、霉酚酸酯及甲泼尼龙预防排斥反应。术后采取抗凝、改善微循环、输注人白蛋白等措施调控患者的出、凝血功能,预防血管吻合口血栓形成和出血,给予法莫替丁或奥美拉唑预防应激性溃疡；给予头孢三代为主的抗生素、更昔洛韦以及氟康唑预防细菌、病毒及真菌感染,并注重对体表易感染部的消毒和护理；术后鼓励患者多下床活动,早期给予谷氨酰胺,尽早将营养支持治疗过渡为肠内营养,以促进移植肠功能的恢复。结果术后3d,1例患者发生肺部鲍曼不动杆菌感染,经抗生素治疗后控制。1例术后5 d移植肠系膜根部出现血肿,手术清除血肿。2例消化道分泌物及大便中发现真菌生长,给予氟康唑治疗后好转。4例在术后20 d左右均发生急性排斥反应,经加大FK506的用量,并以甲泼尼龙冲击治疗后逆转。4例患者,2例获得长期存活,至今分别存活6年8个月和3年2个月,另2例分别于术后5个月、35 d因感染死亡。结论小肠移植术后早期的并发症较多,与小肠的生理结构有关,术后早期并发症的成功防治是临床小肠移植成败的关键。     

Intussesception after jejunoileal bypass as diagnosed by ultrasound

Eighty patients who had undergone jejunoileal bypass for morbid obesity were examined by ultrasound at their routine follow-up visits to the clinic. Ultrasonographic evidence of intestinal intussusception was found in 15 patients (19%). Two of these patients were asymptomatic. Ultrasonographic findings were confirmed by operation in 6 patients (5 with intussusception, 1 negative).     

肠缺血/再灌注致肺损伤时肺内HO-1/CO与iNOS/NO相互作用的研究

目的观察肠缺血/再灌注(I/R)致肺损伤时肺内HO-1/CO与iNOS/NO的相互作用。方法采用肠缺血/再灌注模型。32只Wistar大鼠随机分为假手术组(Sham组)、肠缺血1 h再灌注6 h组(I/R组)、氨基胍组(AG组)和血晶素组(hemin组)。检测肺组织中HO-1和iNOS的表达,观察肺组织丙二醛(MDA)、血清一氧化氮(NO)及动脉血中氧血红蛋白(Hb-CO)的含量,同时观察肺组织病理形态学改变。结果与Sham组比较,I/R组HO-1和iNOS表达显著增强(均P<0.01);AG组HO-1和iNOS表达较I/R组明显降低(均P<0.05);Hemin组iNOS表达较I/R组明显降低而HO-1表达明显升高(均P<0.05);I/R组肺组织MDA、血清NO、血中HbCO较Sham组显著增加(P<0.05或P<0.01);与I/R组比较,AG组、Hemin组肺组织MDA、血清NO显著降低(P<0.05或P<0.01)。AG组的HbCO明显降低而Hemin组的HbCO明显升高(P<0.05)。病理学检查显示,AG组与Hemin组肺组织损伤程度较I/R组明显减轻。结论NO及CO对肠I/R肺组织具有保护作用,两者之间存在着相互作用,肺内HO-1/CO的大量生成具有使NO产生减少的作用,同时iNOS/NO的过量生成具有上调HO-1表达使CO产生增多的作用。     

Hepatic,intestinal and renal transport of 1-naphthol-β-d-glucuronide in mutant rats with hereditary-conjugated hyperbilirubinemia

Summary Recently, a mutant rat strain was described with a genetic defect for the biliary excretion of organic anions (TR^– rats). To determine the possible heterogeneity of the transport systems in liver, intestine and kidney we investigated the transport of the anion 1-naphthol--d-glucuronide (1-NG) in isolated vascularly perfused organ preparations of the rat liver, intestine and kidney of both Wistar rats and TR^– rats. 1-NG was administered as such (liver and kidney experiments) or formed intracellularly from 1-naphthol (1-N) (liver and gut experiments). Independent of the type of exposure to 1-NG, the biliary excretion was considerably impaired in TR^– rats. In the intestine the total appearance and the vascular/luminal distribution pattern of 1-NG were not significantly different from the values in control rats. Furthermore, no significant disturbance was found with respect to the renal clearance of 1-NG in the TR^– rat when compared with the Wistar rat. Thus, the genetic defect in the TR^– rat is restricted to an impaired hepatobiliary excretion of 1-NG and does not affect the excretory systems of the intestine and kidney. These results suggest that the excretion of 1-NG by the liver, intestine and kidney involves distinct organ-specific transport systems.     

GDNF family ligand immunoreactivity in the gut of teleostean fish

Glial-derived neurotrophic factor (GDNF), neurturin (NRTN), persephin (PSPN), and artemin (ARTN) are a group of proteins belonging to the GDNF family ligands (GFLs). GDNF, NRTN, and ARTN support the survival of central, peripheral, and autonomic neuron populations, while PSPN supports the survival of only several central neuron populations. A common receptor, RET, modulates the action of this family and a co-receptor, GFRα, determines RET ligand specificity. GDNF and NRTN appear to be essential for enteric nervous system (ENS) development in mammals, zebrafish, and other teleostean species. GFLs are also essential for the maintenance and plasticity of adult mammalian ENS. In this study, the distribution pattern of GFLs in the intestine of five adult fish (bass, gilt-head, scorpionfish, trout, and zebrafish) was evaluated by immunochemical and immunocytochemical analysis. The results demonstrated the presence of GDNF, NRTN, and ARTN in the gut of all species studied. They appeared to be spread in the ENS and/or endocrine cells of the intestine. These findings suggest that the presence of GFLs in fish gut is not only limited to developmental period, but could be also involved in the enteric physiology of adult species.     

休克大鼠小肠微循环灌流量和血清TNF的变化及多巴胺的作用

在39只失血性休克大鼠中，用激光多普勒微循环血流计及ELISA法测定静脉注射多巴胺前后小肠微循环增流量及血清TNF浓度的变化。结果发现随休克发展，小肠微循环血液灌流量进行性减少，TNF浓度升高。多巴胺（40μg／100gB．W．）治疗可增加小肠微循环血液油流量和降低血清TNF浓度。两者间呈显著性相关（r＝0．897，P＜0．01）。作者认为，多巴胺通过增加小肠微循环血液灌流量，改善肠壁屏障功能，减少内毒素入血，从而降低血清TNF浓度，保护了脏器功能和减轻细胞损伤。     

人体肠道生物力学特性的研究

为探讨人体肠道的生物力学特性，采用电子拉伸机对人体肠道进行一维拉伸试验。结果表明，人体肠道应力-应变关系为指数函数关系。人体肠道各段的指数系数a值接近，但材料常数C有一定的差异，说明肠道各段应力-应变趋势是一致的。在一定应力下，肠道各段轴向与环向的相对伸长率是不同的，表明人体肠道具有各向异性的特性。在一定应变下，肠道各段的增量弹性模量不同，结肠增量弹性模量相对较小，因而更容易发生变形。本研究为肠道内窥镜机器人的研制提供了理论基础。     

Immunohistochemical study about the Flt-1/VEGFR1 expression in the gastrointestinal tract of mouse, rat, dog, swine and monkey

Fms-like tyrosine kinase 1 (Flt-1) performs a subordinate effector role in mesenchymal angiogenesis and potentially serves an equally important functional role as a self-contained receptor in epithelial cells. In both endothelial cells and epithelial cells, Flt-1/vascular endothelial growth factor receptor 1 (VEGFR1) downstream signalling is involved in regulating cellular processes such as cytoskeletal changes and cellular survival protection. Cellular renewal of the gastrointestinal mucosa is based on these processes and might involve Flt-1/VEGFR1 pathway activities; the molecular mechanisms regulating these cellular dynamics remain unclear. This study was performed to investigate the presence and distribution of Flt-1/VEGFR1 in epithelial cells of the gastrointestinal tract by immunohistochemistry (IHC). Gastrointestinal tissues were taken from eight anatomical sites from mouse, rat, dog, swine and monkey. Present results revealed a cytosolic Flt-1/VEGFR1 staining pattern in mucosal epithelial cells for all investigated species. Non-epithelial structures also displayed a distinct Flt-1/VEGFR1 positivity and included vascular smooth muscle walls, enteric smooth muscle layers, the enteric nervous system and capillary endothelial cells. Diverse intensities of the Flt-1/VEGFR1 binding reaction within each species were observed in the intestinal mucosa with a strong immunoreaction in enterocytes and with a low protein expression in the ileum in most species. Crypt cells in the large intestine were mostly negative for Flt-1/VEGFR1. A peculiar and mainly intranuclear antibody binding reaction was found in Brunner's gland epithelial cells of mouse and rat whereas Brunner's glands of dog, swine and monkey remained completely negative. These results indicate a potential involvement of Flt-1/VEGFR1 in normal restitution of gastrointestinal structures in the species studied. Additionally, intranuclear Flt-1/VEGFR1 antibody binding in Brunner's glands of rodents may suggest a nuclear translocation of the transmembrane VEGFR1 which has not previously been described.