山羊高原重度原发性肺冲击伤模型的建立

目的 建立山羊在海拔4 600 m高原环境下的重度原发性肺冲击伤模型,分析高原重度原发性肺冲击伤的特点,为院前救治提供实验基础。方法 选取健康山羊28只,随机分为3 m组22只,3.5 m组6只,采用8 kg TNT当量新型爆炸物,在相同的环境条件下致伤,观察致伤后山羊肺冲击伤伤情,分别于伤前、伤后1 h、24 h监测山羊生命体征、肌钙蛋白Ⅰ,观察肺大体解剖,测肺组织重量、湿/干比重(W/D)等,对重伤山羊进行院前ABC救治。结果 伤后t≤15 min死亡12只,伤后15 min相似文献   

原发肺冲击伤

炸药、炸弹（含核弹、燃料空气炸弹）、地雷、水雷、锅炉等爆炸时可产生不同强度的冲击波（shockwave）,冲击波超压直接作用于机体所造成的损伤称为原发冲击伤或爆震伤（blast injury）,其中以原发肺冲击伤最具代表性^[1,2]。     

大鼠冲击伤时肺毛细血管内皮细胞超微结构的变化

本实验应用超薄切片、硝酸镧示踪、微血管铸型及冷冻蚀刻等电镜技术,观察了大鼠冲击伤时肺毛细血管内皮细胞超微结构的变化。结果显示,肺毛细血管内皮细胞及其细胞紧密连接明显破坏,其对硝酸镧及甲基丙烯酸甲酯的通透性显著增加。     

山羊持续性心房颤动模型的制作

目的:利用慢性间断快速刺激左心房的方法,建立山羊持续性心房颤动（房颤）模型。方法:在10只山羊的左心房游离壁缝合电极条,在左上肺静脉根部缝合1对电极。将左房的1对电极在体外连接自制刺激器,定期停止刺激,分析电生理指标,直至房颤自发维持超过24 h。超声心动图测量基础状态和房颤持续后心房面积等指标。结果:10只山羊中8只完成研究,在9±5（616）d内诱发出持续超过24 h的房颤。随刺激时间延长,房颤波周长逐渐缩短,肺静脉的房颤波周长短于左心房;房颤持续后心房面积明显扩大。结论:利用自行研制的房颤刺激器间断刺激山羊左心房外膜,可在13周内诱发出自发维持超过24 h的持续性房颤。     

一种实验性大鼠慢性阻塞性肺疾病模型的建立

目的 :建立实验性大鼠慢性阻塞性肺疾病 (COPD)模型。方法 :采用香烟染毒和细菌内毒素 (LPS)气管注入的复合方法 ,模仿人类COPD发病的慢性过程 ,制造大鼠慢性阻塞性肺疾病模型。结果 :COPD模型肺组织平均肺泡面积较健康对照组明显增大 ,OD值明显减少 (P <0 0 1)。COPD模型组吸气阻力较健康对照组显著升高 ,肺顺应性 (CLd)及第 0 3s用力呼气量 (FEV0 3)与用力肺活量的比值(FEV0 3 FVC % )较健康对照组显著降低 ,表明有通气阻塞现象 (P <0 0 1)。结论 :本组大鼠COPD模型病理形态学改变和肺功能均与人类慢性阻塞性肺疾病的改变基本一致     

脊柱椎体切除融合山羊模型的建立

目的建立山羊腰椎椎体切除动物模型。方法对15只山羊行盐酸赛拉嗪(陆眠宁)肌肉注射麻醉,行前侧入路腰椎椎体切除钛网植入并钢板内固定术,术后予以青霉素160万U肌肉注射(2次/d),连用3 d。结果成功建模,15只山羊均成活。1例切口感染,予以切口换药处理后痊愈;1例术后双后肢不全性瘫痪,3 d后完全恢复。术后X线拍片示钛网位置较好,固定可靠。术后3个月后将山羊脊柱离体行CT三维重建,观察脊柱融合情况。结论该方法构建动物模型简便、易行,对动物创伤较小,并发症少,CT三维重建能比较准确评估脊柱融合情况。     

半量诱导剂在建立卡氏肺孢子虫肺炎模型中的作用

目前,卡氏肺孢子肺炎（ＰＣＰ）模型的建立虽然可皮下注射可的松的获得稳定的效果,但理传统的诱导剂量存在着致实验动物死亡率高的问题。为此,本文采用减半诱导剂量的方法,既可使ＰＣＰ模型建立,且又明显降低实验动物的死亡率,从而为ＰＣＰ的研究奠定较好的基础。     

Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury

AIM: To study the effects of microcirculation disturbance (MD) on rats with acute severe pancreatitis (ASP). METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2 in lung tissues. We did the same examination in control group. RESULTS: The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased. Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after 1 h and reached its peak value after 9 h. CONCLUSION: MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI.     

冲击伤对大鼠心脏功能的影响

作者用Ｗｉｓｔａｒ大鼠７０只，随机均分为７组，除正常对照组外，其余６组用ＢＳＴ－１型生物激波管致闭合式单纯超压伤。观察幸存大鼠伤后８ｈ到１５ｄ过程中６个时相点离体灌流工作心脏功能的变化。与对照值相比：伤后８ｈ心率减慢至５４％，心缩及心舒期分别延长到１．５和２．０倍；左室内压、＋ｄｐ／ｄｔｍａｘ和－ｄｐ／ｄｔｍａｘ分别降至５４％、３２％、４２％；伤后１周，心率维持在６０％左右，心缩期进行性地延长，可长达１．９倍，心舒期维持在１．６～１．７倍；左室内压及其变化率维持在４６％～６１％；伤后１５ｄ心功能主要指标可恢复到或接近于正常对照水平，自律性恢复早于收缩性的恢复。因此，心脏保护措施宜及早进行，且持之以恒     

重症急性胰腺炎大鼠肺组织中LIF的表达变化及意义

目的:观察重症急性胰腺炎(SAP)大鼠白血病抑制因子(LIF)在肺组织中表达的时相变化, 探讨LIF在SAP病程及肺损伤中的意义．方法:36只♂SD大鼠随机分为正常对照组(N 组,n=6)、假手术组(Sham组,n=6)和重症急性胰腺炎组(SAP组,n=24)．采用胰管逆行灌注50 g/L牛磺胆酸钠的方法复制大鼠SAP模型．用RT-PCR法检测肺组织中LIF mRNA的表达水平,免疫组织化学方法检测NLIF在肺组织中的表达变化．结果:SAP组3 h后肺组织LIF mRNA的表达量明显高于对照组和假手术组(灰度值:1．018± 0．065 vs 1．451±0．067,1．322±0．072,P<0,05), 并且6,12,24 h持续升高(0．853±0．058,0．635 ±0．064,0．582±0．089)(P<0．01)．同样,SAP组 LIF蛋白表达在3和6 h后明显高于对照组和假手术(127．36±2．76,122．53±2．43 vs 159．46 ±2．78,156．35±3．12,P<0．05),并且12,24 h后也维持在很高的水平(109．37±2．87,102．42± 2．27)．结论:LIF作为促炎症因子参与了SAP肺组织的炎症反应．     

大鼠重症急性胰腺炎并发腹内压升高导致肺损伤

目的:探讨大鼠重型急性胰腺炎(SAP)并发腹内压(IAP)增高(IAH)对肺脏的病理损害.方法:健康Wistar大鼠91只,分为假手术组、SAP模型组及SAP IAH组.在不同时间(1,2,4h)SAP模型的基础上,给大鼠不同IAP(2,4,10cmH2O),观察肺脏的功能及组织结构变化.结果:随着腹内压的升高及作用时间的延长,氧分压(PaO2)明显下降、二氧化碳分压(PaCO2)升高,肺组织含水量增加.光镜下可以观察到肺脏间质及肺泡炎性细胞浸润、水肿、出血,肺泡细胞出现空泡化、脱落及衰变等病理改变.电镜下观察到Ⅱ型肺泡上皮细胞核固缩,板层体呈空泡样,线粒体嵴肿胀,形成凋亡细胞等病理改变.结论:SAP并发IAP增高可导致大鼠肺损伤.     

Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats

AIM： To observe the effect of proteasome inhibitor MG-132 on severe acute pancreatitis （SAP） and associated lung injury of rats. METHODS： Male adult SD rats were randomly divided into SAP group, sham-operation group, and MG-132 treatment group. A model of SAP was established by injection of 5% sodium taurocholate into the biliary- pancreatic duct of rats. The MG-132 group was pretreated with 10 mg/kg MG-132 intraperitoneally （ip） 30 min before the induction of pancreatitis. The changes in serum amylase, myeloperoxidase （MPO） activity of pancreatic and pulmonary tissue were measured. The TNF-α level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay （ELISA） kit. Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed. RESULTS： MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-α level, pancreatic and pulmonary MPO activity （P 〈 0.05）. Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity （P 〈 0.05）. CONCLUSION： The proteasome inhibitor MG-132 shows a protective effect on severe acute pancreatitis and associated lung injury of rats.     

莱菔承气汤对重症急性胰腺炎合并肺损伤的治疗作用

目的 观察莱菔承气汤对重症急性胰腺炎合并肺损伤的影响.方法 61例重症急性胰腺炎患者随机分为中药治疗组和常规对照组,中药治疗组在常规治疗基础上给予莱菔承气汤灌肠,对比观察两组患者血气分析指标、血尿淀粉酶、凝血功能指标、影像学检查、体温及白细胞计数恢复正常的时间、排气时间、第一次自行排便时间及APACHEⅡ评分的变化.结果 相同时间内中药治疗组凝血功能指标、影像学检查、血气分析指标及APACHEⅡ评分明显优于常规对照组(P＜0.05);体温,白细胞计数恢复正常的时间,恢复排气排便的时间较常规对照组明显缩短(P＜0.05).结论 莱菔承气汤可明显改善重症急性胰腺炎合并肺损伤患者的状况,其机制可能与促进胃肠功能恢复有关.     

Effect of resveratrol on microcirculation disorder and lung injury following severe acute pancreatitis in rats

AIM: To investigate the mechanism of resveratrol underlying the microcirculation disorder and lung injury following severe acute pancreatitis (SAP). METHODS: Twenty-four rats were divided into 3 groups (SAP, sham and resveratrol groups) randomly. SAP model was established by injecting 4% sodium taurocholate l mL/kg through puncturing pancreatic ducts. Sham (control) group (8 rats) was established by turning over the duodenum. Resveratrol was given at 0.1 mg/kg b.m. intraperitoneally. Rats were sacrificed 9 h after SAP was induced. Blood samples were obtained for hemorrheological examination. Lung tissues were used for pathological observation, and examination of microvascular permeability, dry/wet ratio and myeloperoxidase (MPO) activity. Gene expression of intercellular adhesion molecule-1 (ICAM-1) was detected by RT-PCR. RESULTS: Compared with SAP group, resveratrol relieved the edema and infiltration of leukocytes in the lungs. Resveratrol improved markers of hemorrheology: high VTB (5.77±1.18 mPas vs9.49±1.34 mPas), low VTB (16.12±3.20 mPas vs30.91±7.28 mPas), PV (4.69±1.68 mPas vs 8.00±1.34 mPas), BSR (1.25±0.42 mm/h vs50.03±0.03 mm/h), VPC (54.67±3.08% vs 62.17±3.39%), fibrinogen (203.2?7.8 g/ L vs 51.3±19.1 g/L), original hemolysis (0.45±0.02 vs 0.49±0.02), and complete hemolysis (0.41±0.02 vs 0.43±0.02) (P<0.05). Resveratrol decreased the OD ratio of ICAM-1 gene (0.800±0.03 vs 1.188±0.10), dry/wet ratio (0.74±0.02 vs 0.77±0.03), microvascular permeability (0.079±0.006 vs 0.112±0.004) and MPO activity (4.42±0.32 vs 5.03±0.51) significantly (P<0.05). CONCLUSION: Resveratrol can improve the microcirculation disorder of the lung by decreasing leukocyte-endothelial interaction, reducing blood viscosity, improving the decrease of blood flow, and stabilizing erythrocytes in SAP rats. It may be a potential candidate to treat SAP and its severe complications (ALI).     

氧自由基在肺缺血再灌注损伤中的作用机制

凡是具有未成对电子的原子、分子或原子团都称为自由基，在体内分布广泛。氧自由基的直接损伤作用、以及在介导脂质过氧化、蛋白质和DNA损伤、改变信号传导通路、刺激转录因子活化以及诱导细胞凋亡中有重要而广泛的生物学效应，对肺缺血再灌注损伤的发生、发展和转归有着重要的影响。