不同潮气量通气对海水淹溺致急性肺损伤的炎症抑制作用

目的 观察在治疗海水淹溺所致急性肺损伤时不同潮气量通气对肺炎症的抑制作用.方法 新西兰兔35只,气管内缓慢灌入2ml/kg海水制备海水淹溺致急性肺损伤(SWD-ALI)动物模型.然后随机分为5组(n=7):WD-ALI动物模型组(对照组)及6、8、10、12ml/kg潮气量机械通气组(吸呼比1;2,吸入氧浓度40%,呼气末正压为O,连续通气3h).实验后测定血清及肺泡灌洗液肿瘤坏死因子a(TNF-a)、白介素6(IL-6)水平,并进行肺组织学检查,以评价治疗效果.结果 6ml/kg潮气量机械通气治疗后肺泡灌洗液TNF-a(1.58+0.56 pg/ml)与对照组(1.73±0.81pg/ml)相比明显降低(P＜0.05),余各组机械通气治疗后血清及肺泡灌洗液TNF-a、IL-6水平与对照组比较无明显差异(P>0.05).机械通气后,与对照组相比,各组肺干湿重比均明显增加(P＜0.05),炎细胞浸润均明显好转(P＜0.05).6～8ml/kg潮气量机械通气治疗后肺泡隔断裂无增加,但肺泡萎陷、局灶性肺不张、肺水肿亦无明显好转(P>0.05).12ml/kg潮气量机械通气治疗后肺泡隔断裂明显增加(P＜0.05),肺泡萎陷、局灶性肺不张、肺水肿无明显改变(P>0.05).结论 小潮气量通气策略治疗SWD-ALI能够在一定程度上抑制肺内炎症反应,避免继发肺损伤.     

海水淹溺型急性肺损伤的研究现状

海水淹溺是导致落水人员死亡的主要原因,近年来人们开始重视海水淹溺方面的研究,并在基础研究与临床救治方面均取得了一些成果.在理论和模型制作方面,确立了海水淹溺型急性肺损伤(SWD-ALI)的概念,成功复制出SWDALI动物模型,明确了肺组织的病理及病理牛理改变;在分子生物学研究方而也有大量的报道,为阐明肺损伤机制提供了有力的证据,并通过与淡水淹溺进行对比,发现SWD-ALI具有致伤重、病情进展快的特点,如不给予及时有效的救治,将很快发展为海水淹溺型急性呼吸窘迫综合征(SWD-ARDS);在救治方面,确立了以机械通气为主的综合治疗措施.上述研究成果为以后更全面地认识SWD-ALI、提高海水淹溺伤员的救治成功率奠定了基础.     

海水淹溺型急性肺损伤兔外周血中性粒细胞凋亡的动态变化

目的 探讨海水淹溺型急性肺损伤(SWD-ALI)时外周血中性粒细胞(PMN)凋亡的演变规律以及细胞因子对其可能的影响.方法 36只新西兰兔用随机数字表法均分为对照组(作为Oh基线值)和海水灌注后1、3、6、12、24h组(分别于灌注后1、3、6、12、24h处死).观察各组血象和血气分析指标的变化,计算肺湿/干重比(W/D)和肺微IfIL管通透指数;流式细胞术检测PMN凋亡情况,EIJSA法检测血清TNF-a、IL-1β、IL-10水平;对肺组织进行病理学观察,并计箅病理评分(LPS).结果 W/D值在3h达高峰,肺微血管通透指数以6h最高,炎症细胞浸润以6～12h最显著.LPS在1h已显著高于对照组(P＜0.01),6h达最高.PMN凋亡率于灌注后1h-过性升高,3h显著抑制,6h最低,以后逐渐接近对照水平.PMN计数与凋亡率呈负相关(P＜0.05).各海水灌注组血清TNF-a、IL-1β、IL-10均显著高于对照组(P＜0.05或P＜0.01),与LPS呈正相关(P＜0.05或P＜0.01),但与PMN凋亡率无相关性(P>0.05).结论 PMN凋亡在SWD-ALI炎症反应早期受到显著抑制,是最主要的炎症效应细胞.TNF-a、IL-1β、IL-10在SWD-ALI中发挥重要作用,但对PMN凋亡抑制无显著影响.     

地塞米松对海水淹溺性肺损伤兔肺组织炎症反应的抑制作用

目的了解地塞米松对海水淹溺性肺损伤兔肺组织炎症反应的影响。方法机械通气的麻醉新西兰兔随机分成对照组（CG）和地塞米松治疗组（DG），每组12只。CG兔的气管内灌注4ml／kg体重海水，DG兔在CG的基础上静注1mg／kg地塞米松。取部分右下肺行常规病理学检查。分别用RT-PCR和ELISA检测肺组织中TNF-α、IL-1β和IL-8的mRNA表达及蛋白含量。结果病理学观察显示CG的肺组织内有大量的炎性细胞浸润，肺泡腔内有出血及透明膜形成。DG的上述改变轻于CG。DG肺组织内TNF-α、IL-1β和IL-8的mRNA表达及蛋白含量显著低于CG（P〈0．05）。结论地塞米松治疗可抑制海水淹溺性肺损伤兔肺组织TNF-α、IL-1β和IL-8的表达，减轻肺组织内炎症反应。     

海水淹溺型急性肺损伤兔血管内皮生长因子及其受体的表达

目的 探讨海水淹溺型急性肺损伤(SWD ALI)后血清及组织血管内皮乍长因子(VEGF)及其可溶性受-1(sVEGFR-1)的表达变化及意义.方法 健康成年新西兰兔28只,采用随机数字法均分为对照组和模型组(制作SWD-ALI模型),分别用于3h和6h时间点(每组7只)的观察.分别检测各组动物的肺微血管通透指数、肺湿/干重比和肺组织病理学评分;ELISA法榆测血清、肺泡灌洗液(BALF)及肺组织的VEGF及sVEGFR-1表达,RT PCR法检测肺组织mRNA表达;免疫组化法检测VEGF在肺组织的分布.结果 海水淹溺后,肺组织湿/干重比、肺微血管通透指数均增高,肺组织病理损伤重,6h时点肺组织湿/干重比略低于3h.而肺组织病理学积分仍高于3h.血清中VEGF和sVEGFR-1水平均明显升高,并与损伤时间(r=0.837,r=0.761,P＜0.01)和病理积分呈正相关(r=0.796,r=0.839,P＜0.01).VEGF和sVEFR-1在肺组织及BALF中的表达均明显减低,两者mRNA的表达也明显减低,6h时有所回升.免疫组化提示VEGF在对照组大量表达,分布均匀,淹溺后表达明显减少,分布不均.结论 SWD-ALI时,VEGF和sVEGFR-1表达异常,两者变化规律一致,其水平与肺损伤的程度相关.     

海水淹溺型肺损伤后一氧化氮的表达及地塞米松的干预作用

目的 观察海水淹溺型兔肺损伤后一氧化氮(NO)的变化及不同剂量地塞米松的干预作用,了解地塞米松对海水淹溺型兔肺损伤的作用.方法 兔经气管注入海水,制备海水淹溺型肺损伤兔模型.将35只健康雄性新西兰大白兔随机分为5组:对照组、海水淹溺组、地塞米松低剂量(0.5 mg/kg)、中剂量(1 mg/kg)、高剂量(5 mg/kg)组.海水淹溺组、地塞米松各剂量组于手术稳定20 min后经气管插管注入配方海水(2 ml/kg),对照组气管切开后注入等量生理盐水,地塞米松各剂量组同时经颈动脉注入不同剂量的地塞米松.注射地塞米松后1、3、6 h取血,测血清NO浓度,并于注射地塞米松6 h后处死动物,迅速取出肺脏,测定肺湿/干重比、肺泡灌洗液(BALF)蛋白含量、肺组织中丙二醛(MDA)含量、一氧化氮合酶(NOS)活性、超氧化物歧化酶(SOD)活性,在光镜下观察肺形态结构的变化.结果 海水淹溺可以使肺湿/干重比、肺泡灌洗液内蛋白含量、血浆中NO含量、肺组织中NOS活性升高,使MDA含量增加、SOD活性降低,引起肺形态结构的病理变化.地塞米松可减轻海水淹溺引起的肺损伤,但地塞米松各剂量组与海水淹溺组之间未见明显差异.结论 海水淹溺可明显升高兔血清中的NO含量,地塞米松可减轻海水淹溺性肺损伤.     

海水淹溺型急性肺损伤早期肺组织核因子 κB 及相关细胞因子的动态变化

目的探讨海水淹溺型急性肺损伤早期核因子-κB(nuclear factor-kappa B,NF-κB)活性及相关细胞因子动态变化。方法 36只新西兰兔随机分成对照组(0 h)和海水灌注后1、3、6、12、24 h组。灌注组经气管插管灌注2 ml/kg海水。观察各组动物血气分析的变化。计算肺湿干重比值、肺通透指数。以非放射性凝胶迁移实验分析肺组织NT-κB活性,酶联免疫吸附法检测肺组织肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)、白介素(interleukin,IL)-1β、IL-10浓度,同时进行病理学检查,计算肺病理评分。结果与对照组比,海水灌注组氧合指数迅速低至300 mmHg以下,持续时间长达6 h(P<0.01);肺大体标本淤血水肿严重,显微镜下可见炎症细胞浸润等急性肺损伤病理学征象;肺湿干重比于海水灌注后3 h达高峰,肺通透指数及肺病理评分以海水灌注后6 h组数值最高;肺组织NF-κB活性及TNF-α、IL-1β、IL-10表达量显著增高,并于6 h达高峰。海水淹溺型急性肺损伤早期NF-κB活性与TNF-α、IL-1β、IL-10及肺病理评分正相关(P<0.05),TNF-α、IL-1β、IL-10与肺病理评分、肺通透指数亦密切相关(P<0.05)。结论 NF-κB活化在海水淹溺型急性肺损伤早期与细胞因子过度释放密切相关,在肺组织炎症反应和病理损害中起重要作用。     

海水淹溺型肺损伤与淡水淹溺型肺损伤特征的比较

目的 通过复制海水和淡水淹溺型急性肺损伤大鼠模型,比较海水淹溺与淡水淹溺造成的急性肺损伤的特征与区别.方法 90只大鼠用随机数字法分为3组,即对照组、淡水淹溺组和海水淹溺组,每组在吸入淡水或海水后30min、1、2、4、8h时间点进行观察,每个时相点取6只大鼠用于实验.气管内灌注淡水或海水4ml/kg,建立急性肺损伤模型,分别检测动脉血气分析、肺湿/干重比值(W/D)、肺微血管通透性(PVMP)、血清及支气管肺泡灌洗液(BALF)中肿瘤坏死因子α(TNF-α)的含量,并观察肺组织病理变化.结果 大鼠吸入淡水或海水后,动脉血氧分压(PaO2)明显降低(P<0.05),海水淹溺组比淡水淹溺组降低更为明显(P<0.05).海水淹溺组和淡水淹溺组大鼠的肺W/D值、肺PMVP、血清和BALF中TNF-α含量均明显高于对照组(P<0.05),海水淹溺组较淡水淹溺组升高更明显(P<0.05).病理观察显示,海水淹溺组可见肺间质和肺泡水肿,肺组织灶性出血,并有以中性粒细胞为主的炎性细胞浸润;淡水淹溺组病理学改变与海水淹溺组相似,但损伤程度较轻.结论 海水淹溺较淡水淹溺所引起的肺微血管通透性增加更为明显,低氧血症、肺水肿和炎症反应更严重.     

海水淹溺型急性肺损伤早期肺组织核因子-κB及相关细胞因子的动态变化

目的探讨海水淹溺型急性肺损伤早期核因子-κB(nuclear factor-kappa B,NF-κB)活性及相关细胞因子动态变化。方法 36只新西兰兔随机分成对照组(0 h)和海水灌注后1、3、6、12、24 h组。灌注组经气管插管灌注2 ml/kg海水。观察各组动物血气分析的变化。计算肺湿干重比值、肺通透指数。以非放射性凝胶迁移实验分析肺组织NT-κB活性,酶联免疫吸附法检测肺组织肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)、白介素(interleukin,IL)-1β、IL-10浓度,同时进行病理学检查,计算肺病理评分。结果与对照组比,海水灌注组氧合指数迅速低至300 mmHg以下,持续时间长达6 h(P<0.01);肺大体标本淤血水肿严重,显微镜下可见炎症细胞浸润等急性肺损伤病理学征象;肺湿干重比于海水灌注后3 h达高峰,肺通透指数及肺病理评分以海水灌注后6 h组数值最高;肺组织NF-κB活性及TNF-α、IL-1β、IL-10表达量显著增高,并于6 h达高峰。海水淹溺型急性肺损伤早期NF-κB活性与TNF-α、IL-1β、IL-10及肺病理评分正相关(P<0.05),TNF-α、IL-1β、IL-10与肺病理评分、肺通透指数亦密切相关(P<0.05)。结论 NF-κB活化在海水淹溺型急性肺损伤早期与细胞因子过度释放密切相关,在肺组织炎症反应和病理损害中起重要作用。     

海水淹溺机制研究进展

海水淹溺是军队海上训练、作战及非战斗减员的重要原因。海水淹溺后,除少数因喉头、气管反射性痉挛引起急性窒息外,导致死亡的主要原因是海水淹溺肺水肿(PE-SWD)。国外资料显示,海水淹溺1831例中,单纯PE-SWD病死率为5.2%,伴有血压下降者病死率为19.4%,伴有呼吸停止或心脏骤停,病死率则高达44.0%～93.0%。海水淹溺后绝大部分患者均有肺损伤,并继发肺水肿,甚至海水型呼吸窘迫综合征(SW-RDS),从而使病情更加危重,救治极为困难[1-2]。现将海水淹溺机制研究进展作一介绍。1淹溺过程一般而言,发生淹溺时淹溺者均试图呼吸,大部分淹溺者会将少量的水或胃内容物吸入肺内,少部分淹溺者会因咽部反射性喉痉挛而不会吸入水。随着时间的延长,淹溺者呼吸不畅,会引起氧消耗增加和二氧化碳潴留,导致低氧血症、高碳酸血症和酸中毒。在不自觉屏气期,淹溺者吞入的大量水会进入胃肠道。而随着动脉氧分压进一步下降,喉痉挛松弛,也会导致大量水吸入肺内[3]。2淹溺的病理生理学2.1气道、血流动力学尽管有学者对大量的动物淹溺模型进行了研究,但淹溺的确切机制尚不十分清楚,尤其对淹溺后气道和血流动力学改变情况缺乏了解。早期文献认为,淹溺很...     

海水和淡水肺内灌注对兔肺损伤作用的实验观察

Objective To investigate differences in lung injury induced by seawater and freshwater perfusion in rabbits. Methods 21 New Zealand rabbits were randomly divided into the normal group (the control group), the freshwater group and the seawater group. Same amounts of seawater and freshwater were perfused in the lungs of rabbits through tracheal incubation. Changes in the indices concerning symptomatology, blood-gas, hemodynamics, tumor necrosis factor (TNF-α), interleukin 6 (IL-6), histology and lung injury were monitored 3 hours later. Then, the obtained data were analyzed statistically to see the differences in lung lesions of different animal groups. Results Blood-gas analysis, inflammatory factor measurement, lung injury score indicated that seawater and freshwater perfusion could all induce lung injury to a certain extent, and the injury induced by seawater perfusion was obviously severer(P<0.05). Conclusions Lung injury induced by seawater perfusion is severer than that by freshwater perfusion.     

海水和淡水肺内灌注对兔肺损伤作用的实验观察

Objective To investigate differences in lung injury induced by seawater and freshwater perfusion in rabbits. Methods 21 New Zealand rabbits were randomly divided into the normal group (the control group), the freshwater group and the seawater group. Same amounts of seawater and freshwater were perfused in the lungs of rabbits through tracheal incubation. Changes in the indices concerning symptomatology, blood-gas, hemodynamics, tumor necrosis factor (TNF-α), interleukin 6 (IL-6), histology and lung injury were monitored 3 hours later. Then, the obtained data were analyzed statistically to see the differences in lung lesions of different animal groups. Results Blood-gas analysis, inflammatory factor measurement, lung injury score indicated that seawater and freshwater perfusion could all induce lung injury to a certain extent, and the injury induced by seawater perfusion was obviously severer(P<0.05). Conclusions Lung injury induced by seawater perfusion is severer than that by freshwater perfusion.     

海水和淡水肺内灌注对兔肺损伤作用的实验观察

Objective To investigate differences in lung injury induced by seawater and freshwater perfusion in rabbits. Methods 21 New Zealand rabbits were randomly divided into the normal group (the control group), the freshwater group and the seawater group. Same amounts of seawater and freshwater were perfused in the lungs of rabbits through tracheal incubation. Changes in the indices concerning symptomatology, blood-gas, hemodynamics, tumor necrosis factor (TNF-α), interleukin 6 (IL-6), histology and lung injury were monitored 3 hours later. Then, the obtained data were analyzed statistically to see the differences in lung lesions of different animal groups. Results Blood-gas analysis, inflammatory factor measurement, lung injury score indicated that seawater and freshwater perfusion could all induce lung injury to a certain extent, and the injury induced by seawater perfusion was obviously severer(P<0.05). Conclusions Lung injury induced by seawater perfusion is severer than that by freshwater perfusion.     

海水和淡水肺内灌注对兔肺损伤作用的实验观察

Objective To investigate differences in lung injury induced by seawater and freshwater perfusion in rabbits. Methods 21 New Zealand rabbits were randomly divided into the normal group (the control group), the freshwater group and the seawater group. Same amounts of seawater and freshwater were perfused in the lungs of rabbits through tracheal incubation. Changes in the indices concerning symptomatology, blood-gas, hemodynamics, tumor necrosis factor (TNF-α), interleukin 6 (IL-6), histology and lung injury were monitored 3 hours later. Then, the obtained data were analyzed statistically to see the differences in lung lesions of different animal groups. Results Blood-gas analysis, inflammatory factor measurement, lung injury score indicated that seawater and freshwater perfusion could all induce lung injury to a certain extent, and the injury induced by seawater perfusion was obviously severer(P<0.05). Conclusions Lung injury induced by seawater perfusion is severer than that by freshwater perfusion.     

海水和淡水肺内灌注对兔肺损伤作用的实验观察

Objective To investigate differences in lung injury induced by seawater and freshwater perfusion in rabbits. Methods 21 New Zealand rabbits were randomly divided into the normal group (the control group), the freshwater group and the seawater group. Same amounts of seawater and freshwater were perfused in the lungs of rabbits through tracheal incubation. Changes in the indices concerning symptomatology, blood-gas, hemodynamics, tumor necrosis factor (TNF-α), interleukin 6 (IL-6), histology and lung injury were monitored 3 hours later. Then, the obtained data were analyzed statistically to see the differences in lung lesions of different animal groups. Results Blood-gas analysis, inflammatory factor measurement, lung injury score indicated that seawater and freshwater perfusion could all induce lung injury to a certain extent, and the injury induced by seawater perfusion was obviously severer(P<0.05). Conclusions Lung injury induced by seawater perfusion is severer than that by freshwater perfusion.