慢性阻塞性肺疾病大鼠主要脏器γ-GCS活性及其mRNA表达变化

目的:研究慢性阻塞性肺疾病(COPD)大鼠血浆、肺、心、肝、和肾组织中氧化/抗氧化水平,及γ谷氨酰半胱氨酸合成酶(γ-GCS)活性及其表达在各器官组织中的差异和变化。方法:健康雄性Wistar大鼠14只,随机分COPD模型组和对照组,每组7只。采用每日熏香烟和两次气管内滴入脂多糖(LPS)法制作COPD大鼠模型。检测大鼠血浆、肺、心、肝和肾组织中还原型谷胱甘肽(GSH)、活性氧(ROS)、总抗氧化力(T-AOC)和γ-GCS活性。用逆转录-聚合酶链反应(RT-PCR)法检测肺、心、肝和肾组织中γ-GCS mRNA的表达。结果:COPD组大鼠心、肝中GSH、ROS、T-AOC和γ-GCS活性均显著增高(P均<0.05),但未显示出明显氧化/抗氧化失衡。肺中GSH和ROS提高,而T-AOC下降明显(P均<0.05),表明提高的GSH不足以抵御氧化作用,明显存在氧化/抗氧化失衡。血清中ROS增高,GSH和T-AOC下降明显,显示系统性氧化/抗氧化失衡。COPD大鼠肺组织γ-GCS mRNA表达较对照组显著增高(P<0.05),而心、肝、肾组织中γ-GCS mRNA表达与对照组无明显差异(P>0.05)。结论:COPD大鼠肺内存在氧化/抗氧化失衡,肺组织是γ-GCS表达的主要部位,在抗氧化损伤中可能发挥重要作用。     

降钙素基因相关肽对脑死亡大鼠肺组织氧化应激的影响

目的观察脑死亡大鼠肺组织的氧化应激反应以及降钙素基因相关肽(CGRP)干预处理对脑死亡大鼠肺组织氧化应激的影响。方法健康Wistar大鼠15只,随机分为3组,即对照组(A组)、脑死亡组(B组)及CGRP处理组(C组),每组5只。A组持续麻醉维持12 h。B组通过呼吸、循环支持维持大鼠脑死亡状态12 h。C组于脑死亡模型建立成功后静脉输注CGRP 3μg/kg,随后给予CGRP 6μg/kg持续输注维持12 h,维持实验动物脑死亡状态12 h。于脑死亡后12 h取肺脏组织,检测MDA含量及超氧化物歧化酶(SOD)活性及肺组织γ-谷氨酰半胱氨酸合成酶(γ-GCS)mRNA和蛋白表达水平。结果肺组织中MDA含量B组高于A组及C组(P<0.05),肺组织SOD活性C组高于B组及A组(P<0.05),肺组织γ-GCS mRNA水平C组>B组>A组,γ-GCS蛋白水平C组>A组>B组,组间比较差异均有统计学意义(均P<0.05)。结论脑死亡可导致大鼠肺组织氧化应激反应增强,抗氧化能力减弱;CGRP可增高脑死亡大鼠肺组织γ-GCS蛋白水平,增高抗氧化能力,抑制氧化应激反应。     

氨基胍对大鼠骨骼肌缺血再灌注肺损伤一氧化氮合酶表达的影响

目的观察骨骼肌缺血再灌注(I/R)肺损伤诱导型一氧化氮合酶(iNOS)及一氧化氮(NO)变化情况,探讨氨基胍(AG)及NO在骨骼肌I/R肺损伤中的作用机制。方法将24只雄性Wistar大鼠随机分为四组,对照组,仅进行常规麻醉,不阻断后肢血流;缺血组,即缺血4 h无再灌注组;I/R组,即缺血4 h后再灌注6 h;I/R+AG治疗组,即缺血4 h后继续再灌注6 h,并于再灌注开始时经尾静脉注射AG(150 mg/kg)。检测血清中乳酸脱氢酶(LDH)、NO含量、肺组织中丙二醛(MDA)含量及iNOS基因在肺组织中的表达情况。结果 iNOS表达对照组不明显;在缺血、IR组呈上升趋势;I/R+AG组表达下调;与对照组比较,其余三组差异显著(P0.05);I/R+AG组与对照组比较差异显著(P0.05)。LDH、NO、MDA含量:缺血、I/R组逐渐升高(P0.05);I/R+AG组相应下降,与I/R组比较差异显著(P0.05)。结论在骨骼肌I/R后肺组织中iNOS、血清中的NO均明显升高,AG可明显抑制iNOS表达上调,降低NO、LDH、MDA含量,通过抑制iNOS降低NO含量,减少肺损伤。     

肺源性一氧化氮过度表达在急性坏死性胰腺炎肺损伤中的作用

目的 探讨肺源性一氧化氮（NO）过度表达对急性坏死性胰腺炎（ANP）肺损伤的影响。方法 将72只成年SD大鼠随机分为三组各24只。ANP组、ANP预处理组（预处理组）逆行性胰胆管注射5％牛磺酸钠建立ANP大鼠模型，对照组注射等量生理盐水。造模前30min，预处理组腹腔注射N-硝基-L-精氨酸甲酯（L-NAME）10mg／kg。造模后1、3、6、12h分别处死大鼠各6只，取肺泡巨噬细胞（AM）检测NO水平及诱导型一氧化氮合成酶（iNOS）mRNA表达情况及TNF-a水平，并行肺组织病理学检查。结果 ANP组肺损伤随时间延长而逐渐加重；AM分泌TNF-a，NO水平逐渐升高，至6h达到高峰，12h回落。AMiNOS mRNA的表达情况与NO的变化趋势相似。预处理组各指标变化趋势与ANP组相似，但各指标均低于ANP组（P均〈0．05）；肺组织髓过氧化物酶（MPO）、支气管肺泡灌洗液（BALF）蛋白含量、肺组织湿／干重值逐渐升高，12h达最高值．动脉血氧分压值逐渐降低。结论 ANP发生后肺泡AM的iNOS表达增强，肺源性NO过量表达，并促进TNF-a大量分泌，加重肺损伤，应用iNOS抑制剂则能减轻肺损伤。     

白藜芦醇对慢性阻塞性肺疾病大鼠模型的保护作用

目的探讨白藜芦醇对丙烯醛雾化吸入构建的慢性阻塞性肺疾病(COPD)大鼠模型肺组织的抗炎抗氧化作用。方法用丙烯醛雾化吸入构建COPD大鼠模型。不同浓度的白藜芦醇(5、15、45 mg/kg)预处理COPD大鼠模型,逆转录PCR法检测不同浓度白藜芦醇对COPD大鼠模型肺组织炎性蛋白酶诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子(TNF-α)mRNA表达影响,用化学比色法检测不同浓度白藜芦醇干预下COPD大鼠模型肺组织中谷胱甘肽(GSH)、脂质过氧化产物丙二醛(MDA)含量变化。结果不同浓度的白藜芦醇显著抑制COPD大鼠模型肺组织一氧化氮合酶(iNOS)、肿瘤坏死因子(TNF-α)的mRNA水平,上调大鼠肺组织中内源性巯醇抗氧化物还原型谷胱甘肽(GSH)水平,减少丙二醛(MDA)含量。结论白藜芦醇通过降低促炎因子水平、上调内源性巯醇抗氧化物含量,从而对COPD模型大鼠肺组织发挥抗炎、抗氧化作用。     

盐酸右美托咪定对氟中毒大鼠肠缺血再灌注后肺损伤的保护研究

目的分析研究盐酸右美托咪定对氟中毒大鼠肠缺血再灌注后肺损伤的保护效果。方法抽取84只雄性SD大鼠,随机分为右美托咪定对照组(n=7)、正常对照组(n=7)、氟染毒组(n=35)、右美托咪定干预组(n=35)。对比各组大鼠肺组织MDA、SOD、CAT、GSH及GSH-Px水平、Nrf2mRNA表达水平和动脉血气指标。结果右美托咪定对照组MDA、SOD、CAT、GSH、GSH-Px水平与正常对照组比较,差异无统计学意义(P0.05);与氟染毒组比较,右美托咪定干预组大鼠在2、6、12h时GSH含量和CAT活力与2、6、12、24h时SOD水平及GSH-Px活力均显著增高,在2、6、12h时MDA水平明显下降(P0.05);氟染毒组及右美托咪定干预组Nrf2mRNA表达在2、6、12h时明显高于正常对照组,右美托咪定干预组Nrf2mRNA表达在6、12、24、48h时明显高于氟染毒组(P0.05);氟染毒组肺组织受损严重,而右美托咪定干预组肺组织受损情况轻于氟染毒组。结论氧化应激损伤是氟中毒后肺损伤的主要机制,盐酸右美托咪定可改善Nrf2表达水平,减少氧自由基生成量,保护肺脏。     

还原性谷胱甘肽对大鼠盐酸吸入性肺损伤的保护作用及其机制探讨

目的 探讨还原型谷胱甘肽（GSH）对盐酸吸入性大鼠肺损伤的保护作用及其机制.方法 30只健康成年雄性SD大鼠随机分为A组（生理盐水吸入组）、B组（稀盐酸吸入致肺损伤组）和C组（稀盐酸吸入＋GSH预处理干预组）.术后6h处死大鼠,取肺组织测定肺湿/干重比、丙二醛（MDA）含量、髓过氧化物酶（MPO）活性、TNF-α及IL-1β水平、病理学改变以及Caspase-3含量变化.结果 稀盐酸吸入后,B组肺组织呈弥漫性出血及水肿,中性粒细胞浸润,肺泡隔明显增厚.与A组比较,B、C组Caspase-3阳性表达、肺湿/干重比、MDA含量、MPO活性、TNF-α与IL-1β含量均明显增加（P均＜0.01）.C组肺组织水肿及炎性程度较B组减轻,Caspase-3表达及MDA、MPO、TNF-α、IL-1β含量也较B组不同程度减少（P均＜0.01）.结论 预先给予大鼠GSH可以有效对抗盐酸导致的吸入性肺损伤,这种保护作用与其抑制氧化应激、降低炎症反应以及抑制细胞凋亡有关.     

罗格列酮对慢性阻塞性肺疾病大鼠模型肺组织氧化应激的影响

目的探讨罗格列酮对慢性阻塞性肺疾病(COPD)大鼠肺组织氧化应激的影响。方法将健康SD大鼠24只随机分为3组。被动吸烟和气管内滴入脂多糖(LPS)复制COPD大鼠模型,模型组不进行治疗,罗格列酮组灌胃罗格列酮,对照组为正常大鼠。结果制备肺组织匀浆,用试剂盒测定肺组织匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)和一氧化氮(NO)含量。罗格列酮组大鼠肺组织中MDA含量较模型组明显降低,治疗组大鼠肺组织中SOD、NO含量较模型组明显增加。结论过氧化物酶体增生剂激活的受体(PPARγ)激动剂罗格列酮可明显减轻COPD大鼠肺组织的氧化应激反应,并提高其抗氧化能力。     

香烟烟雾提取物影响肺泡上皮细胞谷胱甘肽和γ谷氨酰半胱氨酸合成酶的表达

香烟中含有大量的氧化剂，吸烟可导致肺内氧化/抗氧化失衡，并最终导致慢性阻塞性肺疾病(COPD)。谷胱甘肽(GSH)是肺内一种重要的抗氧化剂，在氧化剂介导的肺部炎症和肺损伤中起着重要的防御作用。本组研究系统观察香烟烟雾提取物(CSC)对大鼠肺泡上皮细胞(CCIA49)GSH及其合成限速酶γ谷氨酰半胱氨酸合成酶(γ-GCS)表达的影响，旨在深入探讨吸烟引起慢性气道炎症的机制。     

木樨草素对高脂血症模型大鼠血浆一氧化氮水平与抗氧化能力的影响

目的探讨木樨草素对高脂血症大鼠血浆一氧化氮(NO)水平及氧化应激的影响。方法给予高脂血症大鼠木樨草素后检测其血浆NO含量、诱导型一氧化氮合酶(iNOS)及抗氧化能力。结果木樨草素可显著降低高脂血症大鼠血浆NO水平、iNOS活力,明显增加血浆总抗氧化能力(T-AOC),提高血浆谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)活力,显著降低血浆丙二醛(MDA)含量。结论木樨草素可以降低高脂血症大鼠血浆NO水平,与其提高机体抗氧化能力有关。     

Drug-induced mononucleosis-like hepatic injury in a patient with systemic lupus erythematosus

A case of systemic lupus erythematosus (SLE) with mononucleosis-like hepatic injury was described. An emergent cesarean section was performed in a 25 yr-old house wife at 34 weeks gestation, followed by administration of several antibiotics. After the surgery she complained of high fever, hepatomegaly and dull right hypochondralgia, and mild liver dysfunction was also found. The liver biopsy showed prominent mononuclear cell infiltration in the sinusoids with minimum hepatocellular necrosis and mild triaditis, resembling hepatic lesion in infectious mononucleosis (mononucleosis-like injury). There were no clinical and serological features suggestive of infectious mononucleosis. This hepatic lesion was thought to be a manifestation of allergic reaction to drugs to which the lymphocyte stimulation test was found to be positive. Immunological abnormalities inherent in SLE might be related to occurrence of such allergic drug reaction.     

Contrast administration in pediatric cardiac catheterization: Dose and adverse events

Background: In pediatrics, contrast‐related AE such as allergic reactions, seizures, and nephropathy have been reported to occur after cardiac catheterization, but their incidence remains unknown. Objective: We sought to report adverse event (AE) rates attributed to contrast administration in a pediatric cardiac catheterization lab and identify characteristics related to higher doses. Methods: A single institution prospective cardiac catheterization AE database identified AE in children <18 years old exposed to contrast. All AE were reviewed and classified by relationship to contrast. Medical records for the 50 cases who received highest contrast doses were retrospectively reviewed for AE. Patient and procedural characteristics were compared in the top quartile of contrast dose versus remaining cases. Results: Over 3 years, 2,321 consecutive cases required median 3.9 cm³/kg [IQR: 2.0, 6.0] of contrast. Patients receiving high dose contrast (top quartile) were more likely to be <1 year (51% vs. 24%), weigh <10 kg (66% vs. 29%), have complex 2 ventricle disease (56% vs. 35%), be in a high procedure type risk group (57% vs. 26%), and undergo procedures >2 h (67% vs. 28%), all P < 0.001. Only 2 of 2,321 cases (0.09%, 95% CI 0.01–0.31%) had AE possibly related to contrast. These events were an acute neurological change and transient nephropathy. In 50 cases receiving the most contrast, no AE were attributed to contrast. Conclusion: A large volume pediatric cardiac catheterization lab administered ≥ 6 cm³/kg of contrast in a quarter of cases; however, AE related to contrast exposure were exceedingly rare. © 2008 Wiley‐Liss, Inc.     

An analytical review of vasculobiliary injury in laparoscopic and open cholecystectomy

Objectives

Biliary injuries are frequently accompanied by vascular injuries, which may worsen the bile duct injury and cause liver ischemia. We performed an analytical review with the aim of defining vasculobiliary injury and setting out the important issues in this area.

Methods

A literature search of relevant terms was peformed using OvidSP. Bibliographies of papers were also searched to obtain older literature.

Results

Vasculobiliary injury was defined as: an injury to both a bile duct and a hepatic artery and/or portal vein; the bile duct injury may be caused by operative trauma, be ischaemic in origin or both, and may or may not be accompanied by various degrees of hepatic ischaemia. Right hepatic artery (RHA) vasculobiliary injury (VBI) is the most common variant. Injury to the RHA likely extends the biliary injury to a higher level than the gross observed mechanical injury. VBI results in slow hepatic infarction in about 10% of patients. Repair of the artery is rarely possible and the overall benefit unclear. Injuries involving the portal vein or common or proper hepatic arteries are much less common, but have more serious effects including rapid infarction of the liver.

Conclusions

Routine arteriography is recommended in patients with a biliary injury if early repair is contemplated. Consideration should be given to delaying repair of a biliary injury in patients with occlusion of the RHA. Patients with injuries to the portal vein or proper or common hepatic should be emergently referred to tertiary care centers.     

星形细胞在脑损伤中的双向作用

脑损伤后星形细胞会大量增生 ,这些反应性星形细胞可减轻兴奋性氨基酸毒性的损伤 ,缓冲K+ H+ 离子 ,减轻传递抑制 ,对抗氧化损伤和乳酸堆积 ,从而发挥有益的作用。同时 ,这些反应性星形细胞可能参与了脑损伤后的炎症级联反应 ,引起继发性损伤 ,大量增生的星形胶质成为轴突再生和突触重建的障碍 ,从而影响脑损伤后的功能恢复。     

淀粉样变性患者临床特征分析

目的总结淀粉样变性患者的临床特征，指导临床相关诊疗。 方法回顾性分析北京佑安医院2009年1月至2017年12月期间收治的12例经病理活检确诊的淀粉样变性患者的临床资料，并进行总结分析。 结果12例淀粉样变性患者中，男9例、女3例，年龄范围39～70岁，平均(56±8)岁。临床表现方面：乏力5例、纳差4例、腹胀6例、腹痛6例、腹水6例、肝大6例、脾大4例。实验室检查方面：肝功能异常6例，转氨酶异常4例、胆红素升高4例、γ-谷氨酰转肽酶升高10例、碱性磷酸酶升高10例、低白蛋白血症8例、蛋白尿8例、血尿2例、贫血6例、肌酐增高8例。 结论淀粉样变性多见于男性，临床表现多样，多合并肝、肾功能损伤。该疾病主要通过病理活检确诊。