舒芬太尼或芬太尼混合罗哌卡因用于剖宫产术后硬膜外镇痛的效果比较

目的比较舒芬太尼或芬太尼混合罗哌卡因用于剖宫产术后硬膜外镇痛（ PCEA ）效果。方法择期硬膜外麻醉下行子宫下段剖宫产术的患者90例,ASAⅠ～Ⅱ级,随机分为3组（ n ＝30）,3组患者术前于L2～3间隙行硬膜外穿刺,头侧置管3 cm。术后硬膜外镇痛药物成分：S组：舒芬太尼50μg＋罗哌卡因150 mg＋0 Q．9％氯化钠溶液共100 ml;F组：芬太尼0．5 mg＋罗哌卡因150 mg＋0．9％氯化钠溶液共100 ml ;C组：罗哌卡因150 mg＋0．9％氯化钠溶液共100 ml。手术结束前15 min给予格拉司琼3 mg静脉注射,硬膜外导管连接一次性电子止痛泵开始镇痛,背景输注速率均为2 ml/h,PCA剂量2 ml,锁定时间15 min,镇痛时间为50 h。记录术后4 h、8 h、16 h、24 h、36 h（T1～T5）时静息时的VAS评分、Ramsay镇静评分、PCA总按压次数和不良反应。结果与S组比较, T1、T2、T3时 F组和C组VAS评分高（ P ＜0．01）, T3时F组VAS评分低于C组（ P ＜0．01）,有统计学意义,其余时点各组间VAS评分无统计学意义（ P ＞0．05）。与S组比较,PCA总的按压次数S组低于F组和C组（ P ＜0．01）。与S组比较,F组和C组下肢麻木不良反应均增高（ P ＜0．01）,其余不良反应3组间无统计学意义（ P ＞0．05）。术后各时点Ramsay镇静评分3组间无统计学意义（ P ＞0．05）。结论0．5μg/ml舒芬太尼混合0．15％罗哌卡因可安全有效地用于剖宫产术后PCEA,镇痛效果优于5μg/ml的芬太尼混合0．15％罗哌卡因及单纯0．15％罗哌卡因,且不良反应少。     

舒芬太尼或芬太尼复合罗哌卡因对高龄患者人工股骨头置换术后硬膜外镇痛效果观察

目的观察舒芬太尼或芬太尼复合罗哌卡因对高龄患者股骨头置换术后硬膜外镇痛效果。方法拟行人工股骨头置换术高龄患者60例,ASAⅡ～Ⅲ级,70～90岁,体质量45—80kg,分为两组：芬太尼．罗哌卡因组（F组）,舒芬太尼-罗哌卡因组（s组）,每组30例。术毕连接硬膜外镇痛泵,其中F组采用0．125％甲磺酸罗哌卡因200ml＋芬太尼4μg／ml,S组采用0．125％罗哌卡因200ml＋舒芬太尼0．5μg／ml。背景输注剂量4ml／h,单次给药量2ml,锁定时间30min。采用视觉模拟评分法（visualanaloguescale,VAS）和改良OAA／S评分法分别评估镇痛效果和镇静情况;观察患者镇痛满意度;观察恶心、呕吐、皮肤瘙痒、低血压、呼吸抑制等不良反应发生情况。结果03S组的VAS评分低于F组,S组术后12h、24h、48h的OAA／S评分低于F组（P〈0．05）;S组满意度优于F组（P〈0．05）。②两组均未见呼吸抑制发生,s组恶心、呕吐、皮肤瘙痒等不良反应发生率低于F组（P〈0．05）。结论0．5μg／ml舒芬太尼复合0．125％罗哌卡因应用于高龄患者股骨头置换术后硬膜外自控镇痛效果优于4μg／ml芬太尼复合0．125％罗哌卡因,且不良反应发生率低。     

0．2％罗哌卡因复合芬太尼镇痛液持续硬膜外给药临床观察

目的观察0．2％罗哌卡因复合芬太尼2、3、4ml／h用于硬膜外术后镇痛（PCEA）对运动神经阻滞后恢复和镇痛效果。方法选择250例择期脊柱手术病例,均采用硬膜外麻醉。以0．2％罗哌卡因复合芬太尼镇痛液（0．2％罗哌卡因150ml＋芬太尼0．3mg）持续硬膜外给药。按给药速度分为3组,A组：2ml／h;B组：3ml／h;C组：4ml／h。全部病例无按压PCEA泵,采用视觉模拟评分对疼痛进行评分。结果术后48h不同阶段VAS评分,B组、C组低于A组（P〈0．05）;B组和C组差异无统计学意义（P〉0．05）。结论0．2％罗哌卡因复合芬太尼（含罗哌卡因6mg/h,芬太尼6μg/h）背景剂量3ml／h是国人PCEA镇痛最佳选择。     

右美托咪定复合舒芬太尼及罗哌卡因硬膜外术后镇痛对下肢骨科手术应激反应和凝血功能的影响

目的：观察右美托咪定复合舒芬太尼及罗哌卡因硬膜外镇痛对下肢骨科手术应激反应和凝血功能的影响。方法择期行下肢骨科手术患者90例,随机分为D、S1、S2组,每组30例。 D组右美托咪定1．5μg／kg＋舒芬太尼1．0μg／kg＋0．10％罗哌卡因共150 ml,硬膜外镇痛;S1组舒芬太尼1．5μg／kg＋0．10％罗哌卡因共150 ml,硬膜外镇痛,S2组舒芬太尼2．0μg／kg ＋曲马多5 mg／ml 共150 ml,静脉镇痛;3组参数设计,负荷剂量2 ml,背景量2 ml／h,PCA 0．5 ml／次;分别于麻醉前（T0）、术后12 h（T1）、术后24 h（T2）、术后48 h（T3）各时点采集静脉血检测血浆肾上腺素（ E）、去甲肾上腺素（ NE）、皮质醇（ COR）、活化部分凝血活酶时间（ APTT）、凝血酶原时间（ PT）、凝血酶时间（ TT ）、血浆纤维蛋白原（ FIB）值,并于术后T1、T2、T3各时间点对患者进行视觉模拟疼痛评分（ VAS）。结果3组患者T1、T2、T3各时点VAS评分比较差异无统计学意义（ P ＞0．05）。与D组比较,S1组和S2组T1、T2、T3各时点APTT、PT、TT值显著小于D组（ P ＜0．05）;E、NE、COR、FIB值显著高于D组（ P ＜0．05）;与T0比较,D组T1、T2、T3各时点E、NE、COR、FIB、APTT、PT、TT值比较,差异无统计学意义（ P ＞0．05）,与S1和S2组T1、T2、T3各时点比较,差异有统计学意义（ P ＜0．05）。结论右美托咪定复合舒芬太尼及罗哌卡因硬膜外镇痛对下肢骨科手术镇痛效果确切,可能降低患者的应激反应及改善患者术后凝血功能。     

罗哌卡因胸段硬膜外阻滞对油酸致猪急性肺损伤时PMN及ICAM-1的影响

目的观察胸段硬膜外阻滞对油酸所至猪急性肺损伤（ALI）时肺组织嗜中性粒细胞（PMN）数量及细胞间黏附分子-1（ICAM-1）表达的影响。方法选择14只体重为30~35 kg的健康幼猪,麻醉后经颈内静脉持续输注油酸,直至PaO2＆lt;200 mm Hg。随机分为0.9%氯化钠溶液组（S组）及罗哌卡因组（R组）。S组经胸段硬膜外持续输注0.9%氯化钠溶液,R组经硬膜外持续输注罗哌卡因。模型建立后4 h开胸,行支气管肺泡灌洗,测定支气管肺泡灌洗液（BALF）中细胞总数,PMN百分比,并取小块肺组织观察ICAM-1的表达。结果与S组比较,R组BALF中细胞总数,PMN百分比显著性降低,差异有统计学意义（P＆lt;0.05）,R组ICAM-1表达阳性的细胞较S组明显减少。结论胸段硬膜外阻滞可减少PMN在肺内的聚集和ICAM-1表达,对ALI有一定的保护作用。     

罗哌卡因加小剂量氯胺酮用于骨科下肢手术后硬膜外镇痛的临床观察

目的探讨罗哌卡因加小剂量氯胺酮用于骨科下肢手术术后硬膜外镇痛效果及并发症。方法选择80例ASAⅠ—Ⅱ级择期骨科下肢手术患者。随机分为A、B、C、D4组,每组20例,在硬膜外末次给予0．25％罗哌卡因10ml30min后开始术后止痛。A组,持续给予0．2％的罗哌卡因;B组,持续给予0．3％的罗哌卡因;C组,持续给予0．2％罗哌卡因加接泵前给予硬膜外注入氯胺酮0．4mg／kg;D组,持续给予0．2％罗哌卡因加接泵前给予硬膜外注入吗啡2mg。4组均应用福尼亚恒流镇痛泵（固定速率为5ml／h）。观察术后12h、24h、36h不同时段疼痛评分;下肢运动阻滞程度;嗜睡、恶心呕吐、皮肤瘙痒、呼吸抑制、焦虑、烦躁不安、神经质一系列精神症状等并发症情况。结果A组的镇痛VAS评分明显高,与其他3组之间比较有统计学意义（P〈0．01）,其他3组之间比较无差异（P〉0．05）。B组的运动阻滞程度分级高于其他3组（P〈0．05）,其他3组间无差异（P〉0．05）。D组发生恶心呕吐3例（15．0％）,皮肤瘙痒4例（20．0％）,嗜睡2例（10．0％）,其他3组未发现明显不良反应。结论小剂量氯胺酮加0．2％罗哌卡因行术后镇痛,既可减少罗哌卡因的剂量,又降低不良反应的发生。镇痛效果满意,运动阻滞轻,并发症少。     

罗哌卡因复合芬太尼、舒芬太尼在硬膜外麻醉中的应用

目的比较罗哌卡因、罗哌卡因复合芬太尼、罗哌卡因复合舒芬太尼用于硬膜外麻醉的效果。方法择期行下腹部手术患者60例,随机分为三组：罗哌卡因组（R组）罗哌卡因混合芬太尼组（RF组）罗哌卡因混合舒芬太尼组（RS组）每组20例。R组硬膜外注入0．75％罗哌卡因13ml混合生理盐水2ml,RF组注入0．75％罗哌卡因13ml混合0．2mg芬太尼（2m1）,RS组注入0．75％罗哌卡因13ml混合0．2ug舒芬太尼（2ml）。评价腹部感觉、运动阻滞情况、麻醉效果及不良反应。结果与R组比较,RF、RS组感觉阻滞的起效时间缩短,持续时间延长,运动阻滞和麻醉效果改善（P〈0．05）;各组间下肢运动阻滞的起效时间、持续时间及术中术后并发症的发生率差异无统计学意义（P〉0．05）。结论罗哌卡因混合芬太尼、舒芬太尼均可增强罗哌卡因硬膜外麻醉的效果。     

舒芬太尼复合罗哌卡因腰麻超前镇痛对术后硬膜外镇痛的影响

目的观察舒芬太尼复合罗哌卡因腰麻超前镇痛对术后硬膜外镇痛效果的影响。方法将行妇科手术患者80例随机分为C组和S组,每组40例。两组的麻醉镇痛方法分别为：C组0．5％罗哌卡因3ml腰麻,硬膜外首次剂量为舒芬太尼7．5μg稀释成3ml;S组0．5％罗哌卡因3ml＋舒芬太尼2．5gg／ml腰麻,硬膜外首次剂量为生理盐水3ml。镇痛泵的配制均为：0．125％罗哌卡因＋舒芬太尼0．5μg／ml,背景剂量2ml／h,单次给药剂量为2ml,锁定时间为30min。观察并记录镇痛效果、镇痛药的使用量以及不良反应。结果C组与s组相比VAS评分高和BCS评级低,S组在术后4、8、12、24h的疼痛客观评分较C组低,C组PCEA期间的硬外总进药量（120．47±10．58）ml vs．（104．15±7．83）m1]比s组大,C组患者DI／D2比值大于5的比例（17．5％vs．5．O％）高于S组,S组不良反应少于C组。结论舒芬太尼复合罗哌卡因腰麻超前镇痛能减轻术后疼痛,提高患者的舒适度,减少术后硬膜外镇痛药的需求量,且不良反应发生率低。     

腰麻-硬膜外联合阻滞用于分娩镇痛的研究

目的观察罗哌卡因腰麻-硬膜外联合阻滞（CSEA）和产妇自控硬膜外镇痛（PCEA）在分娩镇痛中的效果和安全性以及对产妇和胎儿的影响。方法ASAⅠ～Ⅱ级拟行自然分娩的单胎足月初产妇40例，随机分为2组，宫口开至3～4cm时，R1组经蛛网膜下腔注入0．75％罗哌卡因0．50ml（3．75mg）＋5％葡萄糖溶液至2．5ml，R2组单独硬膜外镇痛。R1组当腰麻作用消失后，连接PCA泵，经硬膜外给予0．175％罗哌卡因，输注背景速率为6ml／h，锁定时间15min，单次剂量2ml。R2组在孕妇宫口开至3～4cm时行硬膜外穿刺置管连接PCA泵给予0．175％罗哌卡因，方法同R1组，监测VAS评分；新生儿Apger评分及NACS评分；观察产程、镇痛时间及PCA泵用药量及按压次数。结果镇痛起效时间：R1组显著短于R2组，有显著性差异（P〈0．01）；R：组罗哌卡因用药量高于R1组，有显著性差异（P〈0．05）。结论罗哌卡因腰麻-硬膜外联合阻滞用于分娩镇痛效果满意，母婴安全。     

低浓度罗哌卡因腰-硬联合阻滞在椎间盘摘除术的应用

目的观察低浓度罗哌卡因腰麻一硬膜外联合阻滞在腰椎间盘摘除术中的应用效果。方法腰椎间盘突出症40例,分为腰麻一硬膜外联合组（观察组）和硬膜外麻醉组（对照组）各20例。观察组用0．1％罗哌卡因4ml行腰麻后待翻身体位固定后再注入0．2％罗哌卡因5ml于硬膜外,根据麻醉效果及平面分次硬膜外推注0．2％罗哌卡因10～15ml,对照组用2％利多卡因3～5ml和0．75％罗哌卡因5～15ml行连续硬膜外麻醉,观察对照两组起效时间、镇痛和肌肉松弛效果,术中、术毕患者脚、下肢活动情况及麻醉前后循环系统的变化。结果观察组麻醉起效时问明显快于对照组（P〉0．05）,镇痛和肌肉松弛效果两组差异不显著（P〉0．05）,术中、术毕患者脚、下肢活动情况明显优于对照组（P〈0．05）。观察组麻醉后15、30min血压及心率与麻醉前差异不显著（P〉0．05）,而对照组麻醉后15、30min血压及心率较麻醉前显著下降（P〈0．05）。结论低浓度罗哌卡因腰麻一硬膜外联合阻滞的起效时间、术中、术毕患者脚、下肢活动情况及麻醉前后的血流动力学稳定明显优于连续硬膜外麻醉。     

Dexamethasone treatment attenuates early seawater instillation-induced acute lung injury in rabbits.

There is very little evidence on the value of giving corticoids in cases of seawater drowning induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate whether dexamethasone treatment can attenuate seawater instillation-induced acute lung injury in rabbits. Seawater (4 ml/kg body weight) was instilled into the lower trachea of ventilated, anesthetized rabbits. Then these rabbits were assigned randomly 20 min later to receive intravenous injection of 1mg/kg body weight of dexamethasone (dissolving in 2 ml of normal saline) or 2 ml of normal saline. All animals demonstrated immediate drops in arterial oxygen tension (PaO2) and the total thoracic compliance, which were significantly improved after 2 h of dexamethasone treatment. Histopathological study also indicated that dexamethasone treatment markedly attenuated lung histopathological changes, alveolar hemorrhage and inflammatory cells infiltration with evidence of decreasing of myeloperoxidase (MPO) activity and tumor necrosis factor-alpha (TNF-alpha) concentration in lung tissue. In addition, dexamethasone treatment reduced extravascular lung water and lung epithelial-endothelial barrier permeability, up-regulated the expression of surfactant protein-A (SP-A) and alpha-epithelial Na+ channel, and increased Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) activity and Na+/K+-ATPase-alpha1 protein abundance. Thus, these data indicate that dexamethasone treatment might be of benefit in patients with seawater aspiration-induced ALI.     

热毒宁注射液治疗急性肺损伤的临床疗效

目的 观察肺保护性通气联合热毒宁注射液治疗急性肺损伤的临床疗效.方法 59例急性肺损伤（ALI）患者随机对照分为肺保护性通气组（对照组,n=30）和肺保护性通气联合热毒宁注射液治疗组（治疗组n=29）,观察两组的临床生命体征、呼吸（RR）、血气分析等改变,进行PaO2和PaO2/FiO2比较、疗效评价及住院期间病死率统计分析.结果 治疗组患者肺损伤得到控制者21例（72.41%）,与对照组的14例（46.67%）比较差异有统计学意义（P〈0.05）;治疗组PaO2上升,PaO2/FiO2显著上升（P〈0.01）.病死率治疗组为24.14%明显低于对照组的50.00%（P〈0.05）.结论 热毒宁注射液对急性肺损伤肺保护性通气具有改善肺功能作用,并可降低住院病死率.     

Protective effects and mechanisms of mogroside V on LPS-induced acute lung injury in mice

Context: Mogroside V, a compound isolated from Momordica grosvenori Swingle, which belongs to the Cucurbitaceae, is a traditional Chinese medicine reported to have anti-inflammatory potential in murine macrophages and a murine ear edema model.

Objective: To investigate the effects and mechanisms of action of this compound in a model of acute lung injury (ALI) induced by lipopolysaccharides (LPS).

Materials and methods: Female BALB/c mice were treated with commercial mogroside V (2.5, 5 and 10?mg/kg) for 1?h prior to intranasal injection of LPS (10?μg in 50?μl). After 12?h, airway inflammation in the ALI model was determined by the wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity of lung tissue, leukocyte recruitment and cytokine levels in the bronchoalveolar lavage fluid (BALF). Additionally, lung tissue was examined by histology and western blotting to investigate the changes in pathology and the signalling in the presence and absence of mogroside V.

Results: Mogroside V at 5 and 10?mg/kg inhibited airway inflammation induced by LPS as measured by the decrease in the histological changes (44 and 67.3% reduction in lung injury score, respectively), a 28.9 and 55.3% reduction in lung MPO activity, and inflammatory cell counts, interleukin-1β (IL‐1β, 382 and 280?pg/ml, respectively), IL-6 (378 and 232?pg/ml, respectively) and tumor necrosis factor-α (TNF-α, 12.5 and 7.8?ng/ml, respectively) levels in the BALF. Additionally, mogroside V treatment reduced the activation of cyclooxygenase 2 (COX-2), inducible NO synthase (iNOS), and the nuclear factor (NF)-κB.

Discussions and conclusions: Together, these data suggest that mogroside V has the potential to protect against LPS-induced airway inflammation in a model of ALI.     

黄芪注射液对脂多糖致大鼠急性肺损伤后细胞凋亡的保护作用

目的:研究黄芪注射液对脂多糖所致大鼠急性肺损伤(ALI)后细胞凋亡的保护作用,探讨其可能的机制。方法:雄性Wistar大鼠200～250 g 45只,随机分成3组,NS对照组、ALI组和黄芪注射液组。后2组以颈外静脉注射脂多糖5 mg·kg~(-1)致急性肺损伤。分别观察各组呼吸频率、动脉血氧分压(PaO_2),处死后检测肺组织湿/干(W/D)比值,免疫组化法检测肺泡上皮细胞Bcl-2、Bax蛋白表达。结果:NS对照组呼吸频率为(73±s 6)次·min~(-1),PaO_2为(90．0±2．0)mmHg,W/D比值为3．287±0．024, Bax/Bcl-2为0．5±1．0;ALI组与NS对照组相比,呼吸频率增快为(112±6)次·min~(-1)(P＜0．01),PaO_2降低为(46±3)mmHg(P＜0．01),W/D比值升高为5．151±0．023(P＜0．01),Bax/Bcl-2上升为7．8±0．7(P＜0．01);黄芪注射液组与ALI组相比,呼吸频率减慢为(94±4)次·min~(-1)(P＜0．01),PaO_2上升为(84±6)mmHg(P＜0．01),W/D比值降低为4．809±0．014(P＜0．01),Bax/Bcl-2下降为0．1±0．7 (P＜0．01)。结论:黄芪注射液可能通过降低Bax/Bcl-2细胞比例抑制细胞凋亡,减轻脂多糖所致ALI。     

Protective effect of hydroxysafflor yellow A against acute lung injury induced by oleic acid and lipopolysaccharide in rats

This study is to investigate the pharmacological effect and mechanism of action of hydroxysafflor yellow A (HSYA) on acute lung injury (ALI). The rat ALI was induced by oleic acid and lipopolysaccharide (LPS) injection. The incidence of acidosis, PaO2 (arterial blood oxygen pressure), W/D (wet weight/dry weight) and lung index (LI) were measured. Electron microscope and optical microscope were applied to observe lung morphological changes in rat. RT-PCR was used to determine TNF-alpha and ICAM-1 mRNA level. Inhibition effect of HSYA on plasma inflammatory cytokine expression was measured by ELISA. HSYA could alleviate pulmonary edema, reduce acidosis, keep PaO2 from descending, inhibit inflammatory cell infiltration, inhibit rat lung TNF-alpha and ICAM-1 mRNA expression and plasma IL-6 and IL-1beta level elevation. HSYA is an effective ingredient to remit ALI induced by oleic acid and LPS in rat.     

Endotoxin-induced acute lung injury and organ dysfunction are attenuated by pentobarbital anaesthesia

1. Acute lung injury (ALI) as a result of sepsis is a major cause of mortality. Certain anaesthetic agents have been reported to suppress pro-inflammatory cytokines and inducible nitric oxide (NO) synthase (iNOS) activities. We investigated the effects of pentobarbital on ALI and organ functions after the administration of endotoxin. 2. Intravenous (i.v.) pentobarbital (20 or 40 mg/kg) was administered 5 min after lipopolysaccharide (LPS; 10 or 30 mg/kg via i.v. infusion). To avoid hypoxia and/or hypercapnia following anaesthesia, we installed a special chamber connected to a rodent ventilator to provide ventilation with 95% oxygen content and 5% nitrogen. The animal was kept at eucapnic conditions (arterial PCO2 at an average of 38 +/- 2 mmHg). 3. We monitored the arterial pressure (AP) and heart rate (HR). Acute lung injury was evaluated by lung weight changes, protein concentration in bronchoalveolar lavage, and Evans blue leakage. Plasma nitrate/nitrite, methyl guanidine and biochemical factors were determined. Pathological and immunofluorescent examinations were performed to observe the lung changes and to determine the activities of pro-inflammatory cytokines, nitrotyrosine and iNOS. 4. Lipopolysaccharide caused dose-dependent systemic hypotension with an increase in the extent of ALI. The lung pathology included oedema and inflammatory cell infiltration. Accompanying the ALI, LPS elevated plasma nitrate/nitrite, methyl guanidine, blood urea nitrogen, lactic dehydrogenase, creatinine phosphokinase, glutamic transaminase and amylase. The lung tissue content of tumour necrosis factor-alpha, interleukin-lbeta, iNOS and nitrotyrosine was increased following LPS administration. These changes were abrogated by pentobarbital anaesthesia. 5. Our results indicated that pentobarbital anaesthesia significantly augmented the LPS-induced systemic hypotension. However, it attenuated the LPS-induced ALI and organ dysfunctions. This agent also improved the survival rate following LPS at high and low doses. This mechanism may be related to the inhibitory effects on the increases in the production or activity of NO, free radicals, pro-inflammatory cytokines, nitrotyrosine and iNOS.     

Polyethyleneimine and DNA nanoparticles-based gene therapy for acute lung injury

Acute lung injury (ALI) is a devastating clinical syndrome causing a substantial mortality, but to date without any effective pharmacological management in clinic. Here, we tested whether nanoparticles based on polyethylenimine (PEI) and DNA could be a potential treatment. In mouse model of ALI induced by lipopolysaccharide (LPS) (10 mg/kg), intravenous injection of PEI/DNA mediated a rapid (in 6 h) and short-lived transgene expression in lung, with alveolar epithelial cells as major targets. When β2-Adrenergic Receptor (β2AR) was applied as therapeutic gene, PEI/β2AR treatment significantly attenuated the severity of ALI, including alveolar fluid clearance, lung water content, histopathology, bronchioalveolar lavage cellularity, protein concentration, and inflammatory cytokines in mice with pre-existing ALI. In high-dose LPS (40 mg/kg)-induced ALI, post-injury treatment of PEI/β2AR significantly improved the 5-day survival of mice from 28% to 64%. These data suggest that PEI/DNA nanoparticles could be an effective agent in future clinical application for ALI treatment.From the Clinical EditorIn this novel study, PEI/DNA nanoparticles are presented as an effective agent for the treatment of the devastating and currently untreatable syndrome of acute lung injury, using a rodent model system.     

急性肺损伤肺保护性通气及CVVH干预的临床研究

目的评价肺保护性通气及CVVH干预在控制急性肺损伤（ALI）和防治多器官功能障碍综合征（MODS）及降低其病死率中的作用。方法60例ALI患者随机分为肺保护性通气组（A组）和肺保护性通气及CVVH干预组（B组）各30例，比较两组患者呼吸力学、动脉血气及血流动力学的变化，观察两组患者肺及肺外器官功能改善率、机械通气并发症发生率、ICU病死率及其死亡原因等。结果两组患者的年龄和APACHE11评分比较差异无统计学意义（P〉0．05）；A组及B组对ALI患者的呼吸力学、动脉血气及血流动力学的影响均优于A组；肺保护性通气及B组对肺及肺外器官功能改善率明显优于A组，另外，机械通气所致肺损伤的发生率、机械通气相关心肌缺血和心律失常的发生率也均明显下降；B组因多器官功能衰竭（MOF）的ICU病死率为13．33％，明显优于A组（46．64％，P〈0．05）。结论肺保护性通气及CVVH干预能改善ALI患者的呼吸力学、动脉血气及血流动力学，能降低其呼吸机所致肺损伤（VILI）、机械通气相关心肌缺血和心律失常的发生率，在防治MODS及降低ALI患者病死率上有显著的临床效果。     

高温气体吸入致豚鼠急性肺损伤动物模型制备的实验研究

目的 制备高温气体吸入致豚鼠急性肺损伤(ALI)动物模型.方法 选择20只雄性豚鼠随机分为2组,每组10只,其中健康豚鼠为对照组、急性肺损伤豚鼠为实验组.实验组吸入150℃ 高温气体制作豚鼠ALI动物模型,然后处死2组豚鼠并取豚鼠右肺的大体标本,称重计算豚鼠肺湿/干重比(W/D),选取2组豚鼠左上肺组织进行HE染色,利用光学显微镜观察肺组织病理变化情况,及时记录其病理变化的结果 ;对豚鼠动脉血液进行血气分析并比较.结果实验组豚鼠肺组织病理结构呈现明显的急性炎症性改变;实验组豚鼠肺W/D比值显著高于对照组[(5.72±0.31)vs(4.88±0.11),P<0.05];实验组豚鼠pH、PaO2显著低于对照组[(7.02±0.12)vs(7.38±0.04),(98.80±62.60)mmHg vs(177.30±24.70)mmHg,P<0.05],而PaCO2显著高于对照组[(74.70±23.23)mmHg vs(31.10±8.77)mmHg,P<0.05].结论 成功制作豚鼠ALI实验动物模型.该模型达到ALI要求,仿真性能高、重复性好、稳定性高,为今后研究高温气体吸入致ALI的临床及基础研究提供了可靠的动物模型.     

Emodin ameliorates acute lung injury induced by severe acute pancreatitis through the up‐regulated expressions of AQP1 and AQP5 in lung

The present study investigates the ameliorating effects of emodin on acute lung injury (ALI) induced by severe acute pancreatitis (SAP). An ALI rat model was constructed by sodium ursodeoxycholate and they were divided into four groups: SHAM, ALI, emodin and dexamethasone (DEX) (n=24 per group). Blood samples and lung tissues were collected 6, 12 and 24 hours after the induction of SAP‐associated ALI. Lung wet/dry ratio, blood gases, serum amylase and tumor necrosis factor‐α (TNF‐α) were measured at each time point. The expressions of AQP1 and AQP5 in lung tissue were detected by immunohistochemical staining, western blotting and real‐time PCR. As the results show, there were no statistical differences in the levels of serum amylase, lung wet/dry ratio, blood gases indexes, serum TNF‐α and pathological changes between emodin and DEX groups. However, significant differences were observed when compared with the ALI group. AQP1 and AQP5 expressions were significantly increased and lung oedemas were alleviated with the treatment of emodin and DEX. The expressions of AQP1 and AQP5 were significantly decreased in SAP‐associated ALI rats. Emodin up‐regulated the expression of AQP1 and AQP5, it could reduce pulmonary oedema and ameliorate SAP‐induced ALI. Regulations on AQP1 and AQP5 expression had a great value in clinical application.