Compartment syndrome. Exclusively the result of increased pressure in the muscular compartment?

Summary The compartment syndrome (cs) is characterized by an increased tissue pressure in a limited space. Pathophysiologically, it is a multifactorial disease that is potentially induced by an initial trauma and develops according to the existence of cofactors. Cofactors are, for instance, the circulation of the patient and the initial treatment of the impending cs. In particular, the microcirculation is altered with endothelial destruction, development of a capillary leak, protein loss from intravasal space and the development of an interstitial and intracellular third space. An impaired drainage of the lymphatic and venous system causes a venous infarction. An arterial infarction results if the tissue pressure exceeds the arteriolar pressure. An accompanying ischemia reperfusion mechanism increases the trauma load. In disadvantageous cases, the patients are in danger of developing a multi-organ deficiency syndrome (MODS) by an uncontrolled inflammatory reaction, by intravasal volume loss and by a myonephropathic systemic reaction. Clinically, the patients suffer a disproportionate amount of pain, followed by neurological signs. Especially in noncompliant patients, tissue pressure measurement is useful. Resuscitation of the circulation as well as splitting of casts is important. In case of a manifest cs, dermatofasciotomy has to be performed as an emergency operation. Even if cs is diagnosed early and fasciotomy is carried out early, the development of sequellae cannot be avoided in every single case.      

环孢素A体外抗曼氏血吸虫雄虫的电镜观察

MF1小鼠感染曼氏血吸虫六周后,经主动脉和门静脉灌注收虫.配对的成虫暴露在不含环孢素A及分别含有1微克/毫升、10微克/毫升、20微克/毫升的环孢素A的199型培养液中体外培养.药物导致的虫体损害分别作扫描电镜和透射电镜观察.药物作用后,雄虫外质膜损伤,外皮层基质出现水肿和空泡,分泌体减少.进行性表皮损害、肿胀以及皮(?)缺损最终导致皮质膜和合胞体的崩溃.本结果表明,环孢素A抗曼氏血吸虫的作用方式是直接的.而外皮质似乎是药物首先攻击的部位.     

大豆蛋白影响肾损害模型钙摄入和钙排出的实验研究

[目的]研究大豆蛋白对肾损害大鼠钙平衡的影响。[方法]选择3月龄断乳雄性SD大鼠40只．按体质量从小到大排序，采用完全随机化原则分为4组。每组10只。标准饲料对照组：喂食含有14％酪蛋白饲料；大豆蛋白饲料组：喂食含有14％大豆分离蛋白饲料；混合饲料1组：喂食含有7％酪蛋白加7％大豆分离蛋白饲料；混合饲料2组：喂食含有7％酪蛋白加14％大豆分离蛋白饲料。实验期用腺嘌呤灌胃共21d，建立肾损害大鼠模型，各组大鼠喂养相应饲料6周，测饲料消耗量、24h尿蛋白、尿钙、钙表观吸收率、储留钙量。[结果]4组实验大鼠饲料摄入量1d～30d无统计学差异，大豆蛋白饲料组和混合饲料1组实验结束时与另外两组相比，尿钙排泄量低，钙表观吸收率和储留钙量高，差异有统计学意义（P〈0．05）。[结论]蛋白质含量水平在14％条件下，含大豆蛋白的两种饲料对肾损害大鼠钙吸收、钙排泄的影响无统计学差异，有利于促进钙吸收，减少钙排泄。     

腹膜透析对重症急性胰腺炎大鼠肾损害的保护作用

目的探讨腹膜透析(PD)对重症急性胰腺炎(SAP)大鼠肾损害的保护作用并探讨可能的机制。方法SD大鼠72只随机分为对照组(24只)、SAP组(24只)和PD组(24只),观察各组血清前列腺素(TXA2/6-K-PGF1a)及内皮素(ET-1)水平和肾脏病理变化。结果SAP组和PD组血清ET-1水平较对照组明显升高,同时段SAP组与PD组比较,PD组水平明显降低;SAP组和PD组血清TXA2/6-K-PGF1a水平较对照组明显升高,同时段SAP组与PD组比较,PD组水平明显降低。PD组大鼠肾病理损害较SAP组明显减轻。结论血液流变异常参与SAP肾损害的发生,早期进行PD治疗对SAP大鼠肾有保护作用,其可能的机制是改善微循环、清除炎症介质等。     

糖尿病肾病患者血液白细胞的变化

目的观测糖尿病肾病患者血液白细胞的变化,分析炎症在糖尿病肾病中的作用。方法对436例糖尿病住院病人,分为糖尿病肾病组(n=102)和糖尿病无肾病组(n=334),检测血液白细胞总数和中性粒细胞数。结果糖尿病肾病组白细胞总数为(7.10±2.21)×109/L,糖尿病无肾病组为(5.61±1.34)×109/L,两组相比,差异有非常显著性意义(t=8.270,P<0.001);中性粒细胞计数值糖尿病肾病组(4.47±2.03)×109/L明显高于糖尿病无肾病组(3.18±1.04)×109/L,差异有非常显著性意义(t=8.481,P<0.001)。相关分析,白细胞数与肌酐(C r)呈正相关(r=0.155,P>0.05)、与尿素(Urea)呈明显正相关(r=0.295,P<0.01)、与血糖(GLU)无明显相关(r=0.055,P>0.05);中性粒细胞与C r、Urea呈明显正相关(r=0.260,0.398,P<0.01)、与GLU呈正相关(r=0.163,P>0.05)。结论糖尿病肾病患者血液白细胞计数升高,与肌酐、尿素水平呈正相关。糖尿病肾病患者存在炎症反应,炎症在糖尿病肾病发生发展中起一定作用。     

Assessment of oxidative DNA damage in the oxyR-deficient SOS chromotest strain Escherichia coli PQ300.

The SOS chromotest is a simple short-term genotoxicity assay measuring the induction of gene sfiA in Escherichia coli K-12. The recent availability of SOS tester strains with additional mutations in DNA repair or protection systems allows testing of DNA damaging compounds for genotoxic specificity. E. coli PQ300 differs from the standard SOS tester strain PQ37 in that it contains an additional mutation in gene oxyR that renders it more sensitive to oxidative genotoxins. The generation of reactive oxygen intermediates (ROI) by hydroperoxides (H2O2, t-butyl hydroperoxide, cumene hydroperoxide), gamma-radiation, glucose oxidase, and xanthine oxidase resulted in a more vigorous SOS response in strain PQ300 compared to strain PQ37. PQ300 was also more sensitive than PQ37 for the detection of reducing agents such as ascorbic acid, cysteine, and glutathione, which also alter the redox status of the bacterial cells. However, intercalating agents (adriamycin, bleomycin, and mitomycin C) and the UV- and radiomimetic compound 4-nitroquinoline-1-oxide whose DNA damaging potential are known also to involve ROI did not show significant differences between strains PQ37 and PQ300. It is concluded that the oxyR-deficient strain PQ300 is useful for detecting certain classes of genotoxins that change the oxidative/antioxidative balance of tester bacteria in the SOS chromotest.     

精神分裂症患者外周血淋巴细胞姊妹染色单体交换的初步观察

检测了18例精神分裂症患者和25例健康人的SCE频率,结果提示患者组SCE频率显著高于对照组,与年龄、性别、病程、临床类型、有无遗传家族史无明显相关。研究提示SCE频率增高似与疾病本身有关。     

活血软坚方对大鼠膜性肾小球肾炎肾小管间质损害影响的实验研究

目的：观察活血软坚方对大鼠膜性肾小球肾炎（MN）肾小管间质损害的影响，并探讨活血软坚中药对MN伴发小管间质损伤的作用机制。方法：用阳离子化牛血清白蛋白复制大鼠MN模型，将实验动物随机分为正常组、模型组、雷公藤组、治疗组，观察24h尿蛋白、血浆白蛋白、胆固醇、三酰甘油、血肌酐、尿素氮等生化指标，并对肾组织进行光镜、电镜、免疫荧光观察；采用RT—PCR的方法检测ColⅠmRNA和ColⅢmRNA的表达。结果：本方能明显降低蛋白尿及血清胆固醇、三酰甘油、血肌酐、尿素氮，升高血清白蛋白，减少免疫复合物沉积，改善肾小球及肾小管的病理损伤。结论：活血软坚方能减轻尿蛋白对肾小管的损伤，减少细胞外基质在肾间质的积聚，减轻肾脏病理损伤，从而达到保护肾功能的作用。     

99mTc-Annexin V检测早期凋亡多巴胺能神经元的实验研究

目的 研究放射性核素标记的膜联蛋白V(Annexin V)与凋亡的多巴胺能神经元的结合特性,探讨使用凋亡显像剂99mTc-Annexin V早期活体显像诊断帕金森病的可行性.方法 采用不同浓度的1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium, MPP+)处理大鼠肾上腺嗜铬细胞瘤细胞(PC12)和人神经母细胞瘤细胞(SH-SY5Y)以诱导其凋亡(PC12 0～200 μm/L, SH-SY5Y 0～500 μm/L),FITC -Annexin V及碘化吡啶(propidiumiodide, PI)双染进行流式细胞仪凋亡检测.以99mTc-Annexin V与凋亡的细胞进行饱和结合实验及细胞摄取实验,研究凋亡细胞与Annexin V的亲和力及其摄取99mTc-Annexin V的动力学.结果 MPP+可诱导PC12细胞及SH-SY5Y细胞发生凋亡,并有明显的量效关系.凋亡细胞可特异性与99mTc-Annexin V结合,亲和力可达(7.16±1.78)nmol/L,每个凋亡的多巴胺能神经元表面的结合位点可达到(179±33)fmol/106cells (PC12)及(220±26)fmol/106cells (SH-SY5Y),且神经元的凋亡水平与其膜结合的99mTc-Annexin V放射性强度有相关性(P＜0.001).结论 凋亡的多巴胺能神经元与99mTc-Annexin V有高度亲和力,其所结合的99mTc-Annexin V放射性强度与细胞的凋亡水平相关,99mTc-Annexin V可用于检测多巴胺能神经元的早期凋亡.