大鼠急性肠缺血后血浆D-乳酸的变化及其与肠粘膜损害的关系

目的观察肠缺血再灌注时门、体循环Ｄ－乳酸的动态变化及其与肠粘膜损害的相关性。方法采用大鼠肠系膜上动脉阻断７５分钟后松夹进行重灌注的模型，分别于术前，阻断末，松夹后０．５，２，６小时活杀动物，观察门静脉和体循环Ｄ－乳酸水平、血浆内毒素含量及小肠病理形态学改变。结果肠缺血７５分钟后大鼠门静脉Ｄ－乳酸水平较伤前值显著上升（Ｐ＜０．０５），再灌注后呈进一步持续升高趋势。外周血Ｄ－乳酸的改变与门脉血基本一致，各时相点与门脉血含量相比差异无显著意义（Ｐ＞０．０５）。相关分析结果显示，门静脉血浆Ｄ－乳酸含量与肠粘膜损伤评分值呈显著正相关（ｒ＝０．４１５，Ｐ＜０．０１）。与此同时，大鼠肠缺血７５分钟门静脉内毒素含量迅速上升，再灌注后２小时达峰值。结论急性肠缺血再灌注可致肠粘膜屏障破坏，使门、体循环Ｄ－乳酸水平显著升高，其含量与小肠粘膜损害密切相关。因此，Ｄ－乳酸可作为新的血浆标志物应用于急性肠粘膜损害的早期诊断     

直肠癌旁移行粘膜增殖活性及其在保肛手术中的意义

目的:探讨直肠癌旁移行粘膜(TM)病理学性质及保肛手术肠管切除范围。方法 应用免疫组化及粘液组化方法观察了81例直肠癌及癌旁粘膜的增殖细胞核抗原(PCNA)表达情况及癌旁TM的变化规律。结果:在癌旁TM、非典型增生及癌组织PCNA呈递增表达,与正常粘膜差异非常显著(P<0.01)。癌旁TM范围在粘液癌明显大于乳头状癌及管状腺癌(P<0.01)。癌旁TM范围在粘液癌明显大于乳头状癌及管状腺癌(P<0.01),在Dukes C期明显大于Dukes A、B期(P<0.01、P<0.05)。结论 直肠癌旁TM具有一定的恶性潜势,直肠癌旁TM的范围与直肠癌的类型及进展密切相关。     

Age-Related Decline of Bone Mass and Intestinal Calcium Absorption in Normal Males

Although about 25% of all hip fractures occur in men, little is known about the pattern of their age-related bone loss and its main determinants. The aim of this cross-sectional study was to evaluate the age-related changes of intestinal calcium absorption, bone mass, and bone turnover in normal men. In 70 normal males (age 17–91 years), we measured spinal and forearm bone density (FBD) (by DXA), fractional intestinal calcium absorption (by oral test), serum immunoreactive parathyroid hormone (PTH), dietary calcium intake (diet records), biochemical markers of bone turnover (serum alkaline phosphatase (ALP), osteocalcin, urine calcium, creatinine, and hydroxyproline), and 1,25(OH)₂D₃ serum levels. Vertebral bone density (VBD) showed a modest decline before age 50 and a greater decline after age 50, whereas FBD presented a significant decrease with advancing age starting at age 40, suggesting a predominant age-related cortical bone loss. Intestinal calcium absorption (⁴⁷CaFA) and serum 1,25(OH)₂D₃ also presented an age-related decline similar to FBD. Simple correlation analysis revealed that age was significantly related to ⁴⁷CaFA (r = 0.60), calcium intake (r = 0.32), VBD and FBD (r = 0.79 and 0.63, respectively), serum 1,25(OH)₂D₃ (r = 0.69), and serum iPTH (r = 0.72). No significant correlation was found between age and biochemical markers of bone remodeling. Partial correlation and stepwise variable selection analyses, using ⁴⁷CaFA and bone mass as dependent variables, showed that in normal males, serum 1,25(OH)₂D₃ and dietary calcium intake were the main contributors (64%) to ⁴⁷CaFA variability, whereas only age accounted for 63% of VBD and age and dietary calcium accounted for 45% of FBD variability. These results indicate that bone loss in men accelerates after age 50 years and that among other factors, intestinal calcium malabsorption and 1,25(OH)₂D₃ serum levels play a role. Received: 19 November 1996 / Accepted: 26 January 1998     

Phenotypic and functional characteristics of intestinal intraepithelial lymphocytes during acute rejection of small intestinal allografts

Infiltration of a transplanted organ by host lymphoid cells is the hallmark of acute rejection. However, after intestinal transplantation, physiological lymphocyte migration may lead to host cell infiltration of the graft even in the absence of rejection. It is unclear whether this lymphocyte migration also involves the intraepithelial compartment of the graft or whether infiltration there is indicative of acute rejection. We demonstrate here that host cell infiltration of the intestinal mucosa occurs both during acute rejection of a small bowel allograft and, to a lesser extent, when rejection is prevented by immunosuppression with FK506. The infiltrating host cells consisted of CD3 ⁺ T cells with a predominant CD4^–CD8 ⁺ phenotype resembling intraepithelial lymphocytes (IELs). Functional studies showed that the nonspecific cytolytic activity of IELs was not affected by acute rejection or by immunosuppression with FK506. These findings indicate that host cell infiltration of the intestinal mucosa does not connote an ongoing acute rejection. Furthermore, the decreased mucosal barrier function during acute rejection of intestinal allgrafts is probably not due to impaired cytolytic activity of IELs. Received: 10 March 1997 Received after revision: 6 November 1997 Accepted: 19 November 1997     

阻塞性黄疸对肠道细菌及小肠粘膜组织的影响

为探讨阻塞性黄疸（简称阻黄）对肠道细菌及粘膜组织的影响，通过建立阻黄动物模型，观察阻黄大鼠肠道细菌移位以及小肠粘膜组织学变化。结果发现：阻黄组（ＢＤＬ）术后３周厌氧性细菌移位的阳性率（４３．７５％）显著高于假性手术组（ＳＬ）（０％），Ｐ＜０．０５；组织学检查显示ＢＤＬ组肠粘膜发生了实质性损害。提示：阻黄时肠道内胆盐缺乏导致肠道常驻菌过度繁殖，肠道粘膜屏障的损害以及机体免疫功能抑制可能是促进肠道细菌移位，导致阻黄时感染易感性增高的主要原因     

开腹手术后麻痹性肠梗阻发生危险因素分析

目的对开腹手术后麻痹性肠梗阻发生的危险因素进行分析。方法回顾性分析2011年1月至2014年12月730例接受开腹手术治疗患者临床资料,采用回归分析方程确定麻痹性肠梗阻发生的危险因素。结果开腹手术患者并发麻痹性肠梗阻发生率为5.6%。单因素分析显示年龄≥60岁、手术时间≥3 h、低蛋白血症、肠粘连范围广、疾病恶性程度和术后白细胞计数≥10×109/L患者麻痹性肠梗阻发生率高,差异具有统计学意义(χ2=5.452、5.295、10.365、9.527、4.905、10.442,P0.05)。多元回归分析显示腹部手术史、手术时间长、肠粘连范围广和无肠道准备是开腹手术后麻痹性肠梗阻发生的危险因素(P0.05)。结论腹部手术史、手术时间长、肠粘连范围广和无肠道准备是开腹手术后麻痹性肠梗阻是麻痹性肠梗阻发生的危险因素,临床工作中应当对上述患者予以干预。     

Intestinal Conditioning After Cardiac Arrest: The Use of Normothermic Extracorporeal Membrane Oxygenation in the Non‐Heart‐Beating Animal Model

The effect of normothermic extracorporeal membrane oxygenation (NECMO) on small bowel preservation in a clinically relevant large animal model of expected donation after cardiac death (eDCD) was evaluated. Thirty domestic crossbred donor pigs were divided into five groups. The first group served as the live donation (LD) group, the second group served as the donation after cardiac death (DCD) group, and the remaining were further assigned into three subgroups: E1 group (1 h NECMO support), E3 group (3 h NECMO support), and E5 group (5 h NECMO support). Pathology, electron microscopy, energy metabolism, cell apoptosis, and tight junction (TJ) protein expression level of intestinal mucosa and the level of plasma d ‐lactic acid were evaluated in normal, cardiac death and at the end of extracorporeal support, respectively. The mean arterial pressure and PaO₂ were maintained over 60 and 267 mm Hg during NECMO support, respectively. One hour of extracorporeal support could improve the energy status in intestines of the DCD group. Although the histologic damage and apoptosis of the E1 group had no significant difference with those of the LD and DCD groups (P > 0.05), the levels of intestinal mucosa TJ protein decreased (P < 0.05), and plasma d ‐lactic acid increased progressively (P < 0.05). With the extension of extracorporeal support, the degree of intestinal mucosa damage and intestinal permeability gradually increased, as well as the content of adenosine triphosphate in intestinal mucosa. The normothermic extracorporeal support for 1 h in DCD is beneficial for improving the energy status and viability of the bowel. However, the integrity of intestinal mucosa was destroyed gradually as extracorporeal support time went by. And the activation of intestinal epithelial apoptosis and hyperoxia might be the factors that lead to intestinal mucosa injury.     

Effects of hypoxia-inducible factor-2α on the expression of tight junction proteins and permeability in rat glomerular endothelial cells under hypoxia condition

Objective To investigate the role of hypoxia-inducible factor-2α (HIF-2α) in the expression of tight junction proteins and permeability alterations in rat glomerular endothelial cells (rGENCs) under hypoxia condition. Methods The expressions of the HIF-2α and tight junction proteins such as occludin and ZO-1 of rGENCs were examined after exposed to 5% oxygen at different treatment time periods (0 h, 12 h, 24 h and 48 h). Then lentiviral transfection was used to knock down HIF-2α expression in rGENCs. The cells were split into four groups, including i) control group where rGENCs were cultured under normal oxygen conditions, ii) hypoxia group, iii) negative control group where rGENCs were infected with a negative vector, iv) HIF-2α lentivirus transfection group. Group ii, iii and iv were kept in hypoxic chamber (5% O2, 5% CO2 and 90% N2) for 24 h. The expressions of occludin, ZO-1 and HIF-2α were assessed by Western blotting. The permeability of rGENCs was measured using trans-epithelium electrical resistant (TEER) by Millicell? ERS voltohmmeter. Results With the elongation of hypoxia time, the expression of HIF-2α was increased gradually, while the occludin expression was decreased, there was statistically significance difference in each group (all P＜0.01). The expression of ZO-1 also decreased gradually under hypoxia circumstance, but no statistically significant was found between 24 h and 48 h groups (all P＞0.05). And a dramatic decrease in TEER of hypoxia cells was detected as compare with control cells (P＜0.01). After knockdown of HIF-2α expression, both expressions of occludin and ZO-1 were increased significantly compared with hypoxia cells (P＜0.01), and TEER elevated at the same time (P＜0.01). Above indexes had no statistical difference between hypoxia cells and negative control cells (all P＞0.05). Conclusion Hypoxia may promote HIF-2α expression, which could increase the permeability of rGENCs by reducing the expression of occludin and ZO-1.     

电离辐射致大鼠肠上皮细胞磷脂变化的研究

目的 观察电离辐射所致肠上皮细胞磷脂的变化,探讨放射性肠损伤的发生机制。方法 将大鼠小肠上皮细胞(IEC-6)分为3组:正常对照组、8 Gy X射线照射组和12 Gy X射线照射组。分别在照射后6和24 h,提取IEC-6细胞磷脂,利用液相色谱-质谱联用技术(HPLC-MS)测定辐射所致细胞磷脂的变化。结果 辐射后6 h,8 Gy照射组细胞磷脂未发生显著变化;12 Gy照射组细胞磷脂变化明显,其中磷脂酰甘油(PG)、磷脂酰肌醇(PI)和溶血磷脂酰胆碱(Lyso PC)均显著性上调(F=5.37、9.60、9.88,P<0.05)。而照射后24 h,两个辐射剂量组中多种磷脂酰乙醇胺(PE)和PG分子显著下调(F=5.15~99.77,P<0.05),12 Gy照射组中多种神经鞘磷脂(SM)显著上调(F=4.35~7.92,P<0.05)。结论 电离辐射可导致大鼠肠上皮细胞(IEC-6)磷脂代谢紊乱,其紊乱程度与辐射剂量相关。     

小肠恶性淋巴瘤的影像诊断(附18例分析)

目的 探讨小肠恶性淋巴瘤的ＣＴ和Ｘ线诊断及鉴别诊断。材料与方法 １８例全部作消化道钡餐造影,其中１２例进行ＣＴ扫描检查。１８例均经手术、病理证实。结果 ＣＴ见肠壁增厚１２例,肠腔扩张与狭窄８例,其中４例单纯狭窄,溃疡２例、腹腔、肝门、脾门淋巴结肿大３例。消化道造影见肠管扩张与狭窄交替１６例,瘘道３例。结论 消化道钡餐造影对小肠恶性淋巴瘤有良好的显示,还可以发现ＣＴ所不能显示的粘膜面,对于估计病变的