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1.
目的探讨早期联用美罗培南(MEP)和大剂量重组人生长激素(rhGH)对严重烫伤免疫抑制大鼠肠源性感染的影响。方法Wistar大鼠54只随机分为对照组、烧伤组和治疗组(C1组、C2组、C3组),后两大组制成25%总体表面积(TBSA)Ⅲ°烫伤免疫抑制模型,伤后2h给予rhGH1.33IU/kg、MEP20mg/kg,伤后8、24h检测门静脉血清内毒素(LPS)、腔静脉血清肿瘤坏死因子-α(TNF-α)含量,肝功能变化和肠道细菌移位率。结果C3(MEP+rhGH治疗)组LPS和TNF-α含量均显著低于其他组(P<0.01),与对照组差异无统计学意义(P>0.05),C3组未发现肠道细菌移位且肝功能检测指标显著低于其他组(P<0.01),与对照组差异无统计学意义(P>0.05)。结论早期联用MEP和rhGH治疗严重烫伤免疫抑制大鼠能显著减轻或防止肠道细菌/内毒素移位,减少炎症介质释放,保护脏器功能。 相似文献
2.
目的:探讨多体位、短间隔及加压追踪法在全消化道钡餐透视检查的应用价值。方法:回顾性分析34例经手术病理确诊或内科治愈或钡餐明确诊断(憩室)的X线表现。年龄12岁81岁,男19例,女15例。采用多体位、短间隔加压追踪法的全消化道钡餐透视检查。结果:空肠近段神经鞘瘤并溃疡出血1例,先天性巨小肠1例,小肠粘连连带压迫空肠近段并不完全性肠梗阻1例,回盲部腺癌并不完全性肠梗阻1例,阑尾切除术后回肠末段肠粘连并不完性肠梗阻1例,美克尔憩室炎并周围溃疡伴不完全性肠梗阻1例,空回肠多发憩室4例,空肠炎9例,回肠炎5例,空回肠炎3例,肠激惹综合征3例。结论:多体位、短间隔加压追踪法全消化道钡餐透视检查,检出率较高,在小肠疾患的检查中有重要的临床意义。 相似文献
3.
大鼠小肠缺血再灌注后血中NO,SOD浓度及肺中Bax,Bcl-2表达的改变 总被引:11,自引:4,他引:7
目的:研究大鼠小肠缺血再灌注后后血中一氧化氮(NO),超氧化物歧化酶(SOD)的浓度变化以及肺组织中Bax,Bcl-2的表达,探讨小肠缺血再灌注后对肺组织的损伤,方法:建立小肠缺血再灌注模型,分对照 ,再灌注后0,30min,1,2h,1,3,7d共8组,于各时点检测血中Bax,Bcl-2的表达情况。结果:大鼠小肠缺血再灌注后NO浓度0min明显升高,2h时降低,随后升高,7d时达高峰,SOD浓度0min明显下降,2h 时升高,随后下降,7d时达最低,Bax,Bcl-2免疫阳性细胞主要位于肺组织中血管内皮细胞和肺泡上皮细胞,再灌注0min,Bax,Bcl-2阳性细胞率增多,30min时Bax,Bcl-2阳性细胞率均升高分别为17.1%和78.1%,Bcl-2表达高于Bax,两者差别显著(P<0.01),2h时降低,其后升高,7d时阳性细胞率达高峰分别为94.1%和83.4%,Bax表达明显高于Bcl-2,两者差异显著(P<0.01)。结论:大鼠小肠缺血再灌注后可引起血中NO,SOD的浓度变化和Bax及Bcl-2阳性细胞在肺组织中的表达改变并可能引起肺组织细胞凋亡和损伤。 相似文献
4.
5.
小肠浆肌膜腔内自体脾组织移植动物模型的建立与意义 总被引:2,自引:2,他引:0
目的探讨增加自体脾组织移植量的方法,提高自体移植脾组织的功能。方法贵州小型香猪3头,经肌注麻醉后剖腹切除脾脏,取脾脏的1/2约150g,切成1mm×1mm×1mm小块备用。在距Treitz韧带50cm处,切取保留肠系膜血管的空肠30cm旷置,再吻合肠管恢复肠腔通道,缝闭肠系膜裂口。旷置空肠等分2段,去除肠粘膜,缝闭一端,将约50g脾组织块分别植于2段肠浆肌膜腔内,缝闭另一端口,妥善固定于肠系膜上。大网膜内移植30g脾组织作为对照观察。结果4个月饲养期间内无肠梗阻发。3段肠浆肌膜腔内脾组织再生良好,组织结构与大网膜内移植脾组织无明显差别,2段再生较差,1段形成脓肿。结论肠浆肌膜腔内移植脾组织的量较大,可作为自体脾组织的移植术式。 相似文献
6.
宜昌市20年结肠镜检查大肠癌患病率回顾性分析 总被引:5,自引:0,他引:5
目的探讨该市大肠癌流行病学和临床特点。方法以所有结肠镜受检对象为研究群体,对大肠癌患病率、大肠癌患者性别、年龄、肿瘤部位进行统计分析;比较大肠癌临床症状与大肠癌患者年龄、肿瘤发生部位的关系。结果自1980年以来,大肠癌年度患病率呈非线性缓慢上升,男性大肠癌患病率7.1%;女性大肠癌患病率5.5%;在3个年限段(80年代、90年代和21世纪5年)大肠癌中位患病年龄分别为男53.5、56.7和59.0岁;女51.9、53.7和55.2岁。986例大肠癌中直肠癌691例,乙状结肠癌82例,降结肠癌18例,脾曲癌4例,横结肠癌37例,肝曲癌30例,升结肠、回盲部癌79例,大肠多发性癌45例。临床症状以便血为主,其次为腹痛、腹部包块和肠梗阻发生率较低,半数以上患者有不同程度贫血。结论该市大肠癌患病率和中位发病年龄呈缓慢上升,低于国内大肠癌高发区。大肠癌肿瘤发生部位有近移和多发趋势。便血是直肠癌主要症状,中老年患者便血发生率高于青年患者,但腹痛发生率低于青年患者。 相似文献
7.
The interactive role of mucosal T lymphocytes in intestinal growth, development and enteropathy 总被引:2,自引:0,他引:2
Abstract Over the past 15–20 years, research has progressively focused on the mucosal T cell as the central factor in the initiation of physiological or pathological changes, first in the growth and maturation of the early (postnatal) intestine, and second in adult-type enteropathies resulting from sensitivity to either food or pathogen-derived antigens. T cell-mediated events may be measured, for example, in terms of specific immunopathologic patterns of change and injury, such as type 1 (lymphocyte infiltration), type 2 (crypt hyperplasia) and type 3 (flat-destructive), which can be recognized and quantitated microscopically; by determination of lymphocyte reactivity through secretion of interleukin-2 receptors (IL-2R) into plasma or expression by mucosal lymphocytes; by quantitation of lymphocyte subsets emigrating into inflamed tissues by immunoperoxidase-labelled monoclonal antibodies; or by the determination of T cell receptor polymorphisms. Alterations in intestinal growth, structure and function at weaning are likely to be T cell-mediated as they are analogous to the same type 1/2 lesions that reflect modulation of adult mucosal architecture in food and parasite-induced hypersensitivity reactions. Enteropathies associated with HIV infection and T cell deficiency display a milder degree of villous flattening and impaired crypt hyperplasia than that typical of gluten-sensitivity, suggesting a reversion to lesser degrees of mucosal pathology (type 1/2). Clearly more information will accrue; meanwhile the remarks in this brief survey should provide a firm basis whereby clinician and scientist can meet, and together recognize and further dissect the modulatory effect of T lymphocytes on mucosal structure and function. 相似文献
8.
M. Nakamura Michitaka Ozaki Shohei Fuchinoue Satoshi Teraoka Kazuo Ota 《Transplant international》1997,10(2):89-95
Ischemia-reperfusion injury by free radicals and lipid peroxides is observed in various organs. Ascorbic acid (AsA) or glutathione
(GSH) in various doses (AsA:2, 0.5, 0.1 mmol/kg, GSH:2 mmol/kg) was intraperitoneally administered to male Wistar rats. The
entire small intestines were resected just before ischemia, after ischemia, and after 20 min of reperfusion (n = 7–10 at each time point). At each time point, the specimens were subjected to assays of lipid peroxides, GSH, and glutaminase
activity of the tissues; they were also examined histologically. In the AsA group, the production of lipid peroxides after
reperfusion was significantly suppressed in a dose-dependent manner, and the ratio of oxidized GSH to total GSH was also significantly
low. Tissue glutaminase activity decreased to a lesser extent, and the degree of injury was apparently less marked in the
AsA group. This study indicates that AsA acts as an antioxidant against peroxidative tissue injury, possibly by scavenging
radicals, preserving reduced GSH, and reducing the peroxidative reaction.
Received: 21 June 1996 Received after revision: 8 October 1996 Accepted: 12 November 1996 相似文献
9.
KETAN A. SHAH SANDRA SHUREY & COLIN J. GREEN 《International journal of experimental pathology》1997,78(5):355-363
Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline ( n = 6) or modified University of Wisconsin solution ( n = 6) at 4 °C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury. 相似文献
10.