兔海水淹溺肺水肿时肺损伤及其机理研究(论著)

目的：观察急性海水淹溺所致肺损伤并探讨其发生机理。方法：向兔肺内灌入海水造成急性淹溺肺水肿模型。采用全自动血气分析仪和计算机图像分析系统，对兔动脉血气、酸碱等６项指标和肺毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶等９项参数进行自动检测和定量测量。结果：灌海水后兔动脉血ｐＨ、ＰａＯ２、血氧饱和度（ＳＯ２）、实际碳酸氢盐（ＡＢ）和碱剩余（ＢＥ）等５项指标明显降低（Ｐ＜０．０１）。ＰａＣＯ２在灌海水后１０～３０分钟呈短暂性升高。在海水淹溺肺水肿（ＰＥ－ＳＷＤ）组中，肺毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶活力显著降低，肺泡Ⅰ、Ⅱ型上皮细胞和肺毛细血管内皮细胞内Ｃａ２＋沉淀颗粒明显增加。结论：低氧血症和代谢性酸中毒可认为是海水淹溺后肺损伤发生的主要原因，细胞内钙超载和肺内Ｎａ＋－Ｋ＋－ＡＴＰ酶活力降低与ＰＥ－ＳＷＤ的发生发展密切相关，应引起临床医生的高度重视     

兔肢体火器伤受海水浸泡后伤道周围骨骼肌Na ＋ / -K ＋ / -ATP酶活性变化

目的观察兔肢体火器伤合并海水浸泡时伤道周围骨骼肌组织Ｎａ＋－Ｋ＋－ＡＴＰ酶（Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ）活性变化及其影响因素,为防治继发损伤提供依据。方法以高速钢珠射击兔后肢,伤后将实验兔随机分为海水浸泡和单致伤组。将浸泡组（１４只）兔浸泡于人工配制的海水中３０分钟,于伤前及伤后３,６,１２,２４小时分别切取距伤道壁０．５ｃｍ（Ａ区）、１．５ｃｍ（Ｂ区）、２．５ｃｍ（Ｃ区）处组织,测定Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ和超氧化物歧化酶（ＳＯＤ）活性、ＡＴＰ和丙二醛（ＭＤＡ）含量。单致伤组（１０只）除不浸泡外,处理同海水浸泡组。结果海水浸泡组各区骨骼肌组织Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性、ＡＴＰ含量均呈伤后３小时较伤前明显下降（Ｐ＜０．０１）,６～１２小时回升,２４小时再次下降的趋势,下降幅度为Ａ区＞Ｂ区＞Ｃ区。ＭＤＡ含量与Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性变化呈负相关（ｒ＝－０．７７Ｐ＜０．０１）。单致伤组上述指标变化趋势同海水浸泡组,但变化幅度小。结论肢体火器伤合并海水浸泡时,可加剧伤道周围骨骼肌组织过氧化脂质反应,抑制抗氧化物酶活性,从而导致能量代谢障碍和细胞膜酶活性下降,加剧继发损伤。     

一氧化氮吸入联合药物对兔海水型呼吸窘迫综合征的预防作用

目的　观察吸入ＮＯ联合药物对海水淹溺肺水肿（ＰＥ－ＳＷＤ）的治疗作用。方法　向兔肺内灌入海水造成急性海水淹溺肺水肿模型后,将兔随机分为３ 个组：（１） ＰＥ－ＳＷＤ模型组,（２） 药物组（采用ＨＦＪＶ和４ 种药物治疗）,（３） 药物和ＮＯ 组（在药物组治疗基础上吸入ＮＯ）。采用全自动血气分析仪和薄板层析测兔动脉血气和酸碱;测定肺泡灌洗液中二棕榈酰磷脂酰胆碱（ＤＰＰＣ）含量与肺组织干／湿重比;观察兔存活时间及海水型呼吸窘迫综合征（ＳＷ－ＲＤＳ）发生率。结果　ＮＯ联合药物组兔动脉血ＰａＯ２ 和ＳａＯ２ 明显高于ＰＥ－ＳＷＤ组,动物存活时间比药物组大大延长,未发生ＳＷ－ＲＤＳ,肺组织切片在电镜下观察细胞损伤明显减轻。结论　ＮＯ联合药物可解除支气管平滑肌痉挛,改善肺通气功能,并可松弛肺血管平滑肌,降低肺血管阻力而提高心功能,阻止ＰＥ－ＳＷＤ向ＳＷ－ＲＤＳ转化。     

高压氧对实验兔海水型呼吸窘迫综合征的预防作用

目的　观察高压氧（ＨＢＯ）对海水淹溺肺水肿（ＰＥ－ＳＷＤ）的预防作用。方法　复制ＰＥ－ＳＷＤ动物模型后,３２ 只兔随机分为ＰＥ－ＳＷＤ对照组、药物治疗组和ＨＢＯ组。对３ 组兔的动脉血气酸碱指标、Ｃａ２＋ 沉淀反应颗粒、ｃ－ｆｏｓ ｍ ＲＮＡ和ｃ－ｊｕｎ ｍ ＲＮＡ 等进行自动检测和定量分析比较,并观察分析３组兔的存活时间和海水型呼吸窘迫综合征（ｓｅａｗ ａｔｅｒ－ｒｅｓｐｉｒａｔｏｒｙ ｄｉｓｔｒｅｓｓ ｓｙｎｄｒｏｍ ｅ,ＳＷ－ＲＤＳ）发生率。结果　ＨＢＯ组兔ＰａＯ２ ,ＳａＯ２ 和ｐＨ ３ 项指标比药物组显著升高（Ｐ＜ ０．０１）,动物存活时间［（４３．０３±７．１９）小时］比药物组［（２３．５８±１．４９）小时］明显延长,Ｃａ２＋ 沉淀反应颗粒,ｃ－ｆｏｓ ｍ ＲＮＡ,ｃ－ｊｕｎ ｍ ＲＮＡ和ＳＷ－ＲＤＳ发生率ＨＢＯ组则明显低于药物组（Ｐ＜ ０．０１）。结论　ＨＢＯ可明显提高ＰａＯ２ 和ＳａＯ２,有效改善低氧血症和代谢性酸中毒,减轻ＰＥ－ＳＷＤ时肺组织的损伤,从而可防止ＰＥ－ＳＷＤ向ＳＷ－ＲＤＳ转化。     

大鼠颅脑液压损伤后脑组织内Na^＋—K^＋—ATP酶活性的变化

目的：测定大鼠颅脑液压损伤后脑组织内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性，探讨其在继发性脑损伤中的作用。方法：利用大鼠颅脑液压损伤模型，在致伤后６小时测定脑组织含水量、脑组织内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性。结果：脑损伤６小时后，损伤侧脑组织内含水量明显增加（Ｐ＜０．０５），Ｎａ＋－Ｋ＋－ＡＴＰ酶活性明显下降（Ｐ＜０．０５）；而未损伤侧脑组织含水量和脑内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性均无显著改变（Ｐ＞０．０５）。结论：脑损伤后脑组织内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性下降是继发性脑损害发生和发展的重要因素之一。     

一氧化氮在烧伤大鼠肾脏损伤中的作用

目的：研究一氧化氮（ＮＯ）在烧伤早期肾脏损害中的变化及意义．方法：动态观察大鼠３０％Ⅲ度烧伤后血浆及肾脏ＮＯ、内皮素（ＥＴ）含量变化，应用外源性ＮＯ载体ＳＩＮ－１以观察其对烧伤早期肾脏损害的影响．结果：大鼠烧伤后肾脏明显受损，伤后血浆及肾组织ＮＯ、ＥＴ含量明显升高，由于ＮＯ升高幅度相对较低，ＥＴ／ＮＯ值也显著增加，肾组织ＥＴ／ＮＯ值改变与肾脏血流量的降低呈显著负相关；伤后在一定的液体复苏下应用ＳＩＮ－１可一定程度恢复肾脏血流量，增加肾组织超氧化物歧化酶（ＳＯＤ）、钠钾三磷酸腺苷（Ｎａ＋－Ｋ＋－ＡＴＰ）酶活性及三磷酸腺苷（ＡＴＰ）、二磷酸腺苷（ＡＤＰ）含量，减少丙二醛（ＭＤＡ）、腺苷酸（ＡＭＰ）含量，减轻肾组织水肿．结论：烧伤后由于肾脏内源性ＮＯ的相对不足，导致肾脏血管收缩，造成肾组织缺血缺氧性损害，继而发生能量代谢紊乱及脂质过氧化损害，外源性补充ＮＯ则可一定程度逆转烧伤后肾脏损害．     

运动病大鼠血浆前列腺素测定和小脑Na~ -K~ -ATP酶图像定量分析(论著)

目的：研究运动病大鼠血浆ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α与毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶的变化规律及其内在联系，探讨运动病发生的机理。方法：采用放射免疫方法和图像分析系统，对运动病大鼠血浆ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α和小脑毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶进行自动检测和定量分析。结果：运动病组大鼠血浆ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１），而小脑毛细血管内皮细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶的活性则显著低于对照组（Ｐ＜０．０１）。结论：血浆中高浓度的ＴＸＢ２可能是运动病脑血管收缩，脑血流量减少的重要原因之一。脑内Ｎａ＋－Ｋ＋－ＡＴＰ酶活力降低既是脑组织缺血缺氧的结果，又是加重运动病脑血流障碍的继发性原因。     

高压氧对缺血再灌注条件下鼠视网膜细胞膜功能的影响(论著)

目的：观察高压氧（ＨＢＯ）对缺血再灌注视网膜细胞膜功能的影响。方法：选择３５只ＳＤ大鼠，随机分为４组：正常组、再灌注组、空气加压组和ＨＢＯ组。采用升高眼内压（ＩＯＰ）致视网膜血管断流造成视网膜缺血模型，然后给予再灌注３小时。其中空气加压组和ＨＢＯ组于再灌注开始后将动物置于ＨＢＯ舱内，在２５２．３８ｋＰａ（≈２．５ＡＴＡ）压力下分别吸空气和纯氧，加压时间为８０分钟。再灌注结束后取眼球制备视网膜细胞膜匀浆液。用定磷法测定视网膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性，用荧光探针ＤＰＨ标记细胞膜并测定其膜流动性。结果：ＨＢＯ组视网膜细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性与正常组比较无显著性差异，而与再灌注组比较有非常显著性差异；ＨＢＯ组膜流动性与再灌注组比较有非常显著性差异。结论：ＨＢＯ对缺血及再灌注所造成的视网膜细胞功能的损伤具有明显的治疗作用。     

烟雾吸入伤后肺表面活性物质蛋白A含量的动态变化及意义

目的探讨烟雾吸入伤后肺表面活性物质蛋白Ａ（ＳＰ－Ａ）含量的变化、可能机理及其与肺表面活性物质（ＰＳ）活性抑制和肺功能损害的关系。方法采用大鼠烟雾吸入伤模型，分别检测正常对照及致伤２ｈ、６ｈ、１２ｈ和２４ｈ动物的动脉血气，肺水量，静态肺顺应性（Ｃｓｔ），支气管肺泡灌洗液（ＢＡＬＦ）表面张力特性，ＢＡＬＦ中ＳＰ－Ａ、丙二醛（ＭＤＡ）、总蛋白（ＴＰ）含量及弹性蛋白酶（Ｅｌａ）活性。结果动物伤后出现急性呼吸衰竭和肺水肿，Ｃｓｔ显著降低；ＢＡＬＦ的最小表面张力（ＳＴｍｉｎ）升高，滞后环面积下降；ＢＡＬＦ中ＳＰ－Ａ、ＭＤＡ、ＴＰ含量及Ｅｌａ活性明显升高，但ＳＰＡ－Ａ的相对含量（％ＴＰ）降低，且与Ｅｌａ、Ｃｓｔ和ＳＴｍｉｎ的变化相关显著。结论烟雾吸入伤早期ＳＰ－Ａ相对含量减少，可能是导致肺表面活性物质活性抑制及肺功能障碍的主要原因之一。氧化及Ｅｌａ可能是引起ＳＰ－Ａ含量和（或）功能异常的重要因素。     

离断肢体血管与肌肉保护的实验研究

目的：研究温度与药物（利多卡因、能量合剂、林格氏液）对离断肢体血管与肌肉的影响。方法：以大鼠断肢为模型，电镜观察超微结构变化，用赵卫国法及Ｇｏｌｄｂｅｒｇ法测定组织内Ｎａ＋－Ｋ＋－ＡＴＰ酶及Ｃａ＋＋－ＡＴＰ酶。结果：低温（０～４℃）、能量合剂灌注对血管和骨骼肌超微结构及酶活性皆明显优于室温及林格氏液灌注，利多卡因灌注仅对血管有益。结论：低温、能量合剂、利多卡因对离断肢体有保护作用     

高压氧、机械通气对海水淹溺肺水肿兔肺组织学及呼吸功能的影响

目的　观察高压氧 (HBO)、机械通气对海水淹溺肺水肿 (PE- SWD)兔肺组织学及呼吸功能的影响。方法　将 2 4只实验动物随机分为 PE- SWD组、HBO治疗组、机械通气治疗组。在不同时间点观察动脉血气分析、呼吸频率、呼吸动力学指标 ,实验结束后进行肺组织病理学检查。结果　 HBO治疗组、机械通气治疗组各相同时间点 Pa O2 明显高于 PE- SWD组 (P<0 .0 1) ;HBO治疗组除个别时间点外 ,p H、Pa CO2 在整个治疗过程中变化不明显 ;机械通气治疗后 p H的变化规律略与 PE- SWD组相同 ,但治疗结束时仍低于其他组 (P<0 .0 1) ,Pa CO2 始终维持在一个较高的水平 (P<0 .0 1)。两种治疗都减轻了肺损伤程度 ,在降低气道峰压、提高肺顺应性方面两治疗组之间比较 ,差异无显著性意义 (P>0 .0 5 )。结论　 HBO和机械通气治疗可明显纠正 PE- SWD时的低氧血症 ,减轻肺损伤程度 ,改善呼吸功能。     

急性肺栓塞后osteoglycin的表达及对胶原代谢的影响

目的 研究大鼠急性肺栓塞模型肺组织中osteoglycin(OGN)的表达变化及其对胶原代谢的影响.方法 建立大鼠急性肺栓塞模型,分别在急性肺栓塞后1、8、24和48h开胸取出肺组织,提取总RNA和总蛋白.以正常大鼠为对照组,采用半定量RT-PCR研究OGN mRNA的表达变化,采用Western blot进一步验证OGN蛋白表达的变化,采用免疫组织化学方法检测肺栓塞前后大鼠肺组织中OGN的表达变化及组织分布情况,采用Masson染色观察急性肺栓塞4周后肺组织内的胶原沉积状况.结果 在大鼠急性肺栓塞后,OGN在mRNA及蛋白水平均逐渐降低.免疫组化染色显示OGN主要分布在支气管黏膜上皮细胞下层、软骨组织和肺泡周围,且在肺动脉内皮细胞下层、外膜和肺静脉的内膜、中膜以及外膜均有分布.急性肺栓塞后OGN在上述组织内的表达均明显降低.急性肺栓塞4周后肺组织内的胶原沉积明显增加.结论 大鼠急性肺栓塞后肺组织内OGN表达降低,促进了胶原在肺部的沉积.     

海水浸泡诱导小鼠肺组织氧自由基的改变及其防护的研究

目的：观察海水浸泡条件下，小鼠肺组织氧自由基的改变及超氧化物歧化酶（ＳＯＤ）的防护作用。方法：选用１２０只小鼠，随机分组，检测其ＳＯＤ活性及丙二醛（ＭＤＡ）含量的变化。结果：除未注射ＳＯＤ的小鼠，在海水浸泡２０分钟组ＳＯＤ活性稍高且无统计学意义外，其余各组ＳＯＤ活性均较相应对照组低，并均有显著性差异（Ｐ＜０．０１），而ＭＤＡ含量变化则相反。注射ＳＯＤ小鼠浸泡不同时间后，其各时间点ＳＯＤ活性均较未注射ＳＯＤ小鼠者高，而ＭＤＡ含量变化则相反并与注射ＳＯＤ的剂量有关。结论：海水浸泡可诱导小鼠肺组织氧自由基的改变，并有可能引起肺组织损伤，而注射ＳＯＤ对小鼠肺组织氧自由基的改变有防护作用。因此，为加强对海水浸泡伤害的防护，使用ＳＯＤ制剂值得推荐。     

大鼠烟雾吸入伤后肺表面活性物质功能活性的变化及作用(论著)

目的：探讨肺表面活性物质功能活性的动态变化与急性烟雾吸入性肺损伤发生发展的关系。法：采用大鼠烟雾吸入伤模型，分别检测了正常对照及致伤2、6、12和24小时动物的动脉血气、肺水量、静态肺顺应性和支气管肺泡灌洗液（BALF）的表面张力活性。结果：动物伤后出现急性呼吸衰竭和严肺水肿，肺顺应性显著降低，以低容量肺顺应性和扩张指数下降早而明显；BALF的最小表面张力进性升高，滞后环面积、稳定指数和恢复系数进行性下降。最小表面张力的变化与静态肺顺应性、PaO2、PaCO2的改变相关显著。结论：烟雾吸入伤早期肺表面活性物质功能活性即显著降低，并可能在呼吸功损害中起重要作用。     

Differential diagnosis between freshwater drowning and saltwater drowning based on intrapulmonary aquaporin-5 expression

The intrapulmonary expression of aquaporin-5 (AQP5) was examined in an experimental drowning model and forensic autopsy cases to discuss the possibility for differentiation between freshwater drowning (FWD) and saltwater drowning (SWD). In animal experiments, mice were classified into four groups: (group I: FWD; group II: SWD; group III: postmortem immersion (PI); and group IV: cervical dislocation as controls. In group I, intrapulmonary AQP5 expression was significantly suppressed at both gene and protein levels, compared with the other three groups, and there was no significant difference in AQP5 expression among groups II to IV. In the next series, we examined AQP5 gene expression in human lung samples obtained from forensic autopsies at less than 48 h postmortem (nine FWD cases, five SWD cases, and 14 other cases). Although AQP5 mRNA could be detected in all lung samples under the employed experimental conditions, the intrapulmonary gene expression of AQP5 in FWD was significantly attenuated compared with the other groups. These observations imply that AQP5 expression in type I alveolar epithelial cells was suppressed by hypotonic water to prevent hemodilution from the physiological aspect. Moreover, the analysis of intrapulmonary AQP5 expression would be forensically useful for differentiation between FWD and SWD, or between FWD and PI.     

Semi-quantitation of pulmonary perfusion heterogeneity on respiratory-gated inspiratory and expiratory perfusion SPECT in patients with pulmonary emphysema

OBJECTIVE: Pulmonary perfusion heterogeneity (PPH) in pulmonary emphysema (PE) was semi-quantified by functional lung volume rate (FLVR) curves obtained from respiratory-gated inspiratory and expiratory single-photon emission computed tomography (SPECT). METHODS: Gated and ungated SPECT were obtained in 36 PE patients [25 with stage IIA and 11 with stage IIB for global initiative for chronic obstructive lung disease (GOLD) stage classification] and 12 controls, using a triple-head SPECT system and a respiratory tracking device. On gated SPECT, the voxel numbers calculated at the 10% cutoff threshold for the maximum lung radioactivity were assumed to be the functional lung volume of the lung (V). FLVR (%) was calculated as FLV divided by V at every additional 10% thresholds, yielding inspiratory and expiratory FLVR curves. The dissociations between these curves (DeltaFLVRinsp-exsp) and the total difference (D index) of these curves from the normal standard curve (averaged inspiratory and expiratory curve in controls) were calculated. D index and the extent of low attenuation area (%LAA) on CT were correlated with the transfer coefficient for carbon monoxide (KCO) in PE patients. RESULTS: Although gated and ungated SPECT showed fairly uniform perfusion in controls, gated SPECT-enhanced PPH compared with ungated SPECT in PE patients, with significantly higher dissociation (DeltaFLVRinsp-exsp) than that in controls (24.9%+/-9.5% vs. 4.5%+/-1.3%; P<0.0001). DeltaFLVRinsp-exsp was significantly higher even in stage IIA patients (P<0.0001). Expiratory D index was significantly higher than the inspiratory one in PE patients (P<0.01). This index was significantly higher in stage IIB patients than in stage IIA patients (44.1%+/-19.0% vs. 29.4%+/-13.7%; P<0.05), and was significantly correlated with KCO (R=0.642, P<0.0001) in all PE patients, although %LAA was not correlated with KCO. CONCLUSIONS: FLVR curve analysis on gated SPECT appears useful for semi-quantitation of respiratory change of PPH in PE. Expiratory D index may better reflect the lung pathophysiology of PE than morphologic CT.     

Assessment of regional lung function impairment in airway obstruction and pulmonary embolic dogs with combined noncontrast electrocardiogram-gated perfusion and gadolinium diethylenetriaminepentaacetic acid aerosol magnetic resonance images

PURPOSE: To define regional function impairment in airway obstruction (AO) and pulmonary embolic (PE) dogs with a combination study of noncontrast electrocardiogram (ECG)-gated perfusion and gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) aerosol magnetic resonance (MR) images. METHODS: After acquisition of multiphase fast-spin-echo (FSE) MR images during cardiac cycles in 14 AO dogs and 19 PE dogs, ECG-gated perfusion-weighted (PW) images were obtained by subtraction between two-phase images of the minimum lung signal intensity (SI) during systole and maximum SI during diastole. Each dog subsequently inhaled Gd-DTPA aerosol for 20 minutes, and subtracted Gd-DTPA aerosol images were obtained from precontrast and maximally enhanced images. ECG-gated PW images were compared with intravenous Gd-DTPA-enhanced pulmonary arterial perfusion phase (PAPP) images. RESULTS: ECG-gated PW images were consistent with Gd-DTPA-enhanced PAPP images in all dogs, with significant correlations in the affected-to-unaffected lung perfusion ratios (P < 0.005). Gd-DTPA aerosol images showed sufficient and uniform enhancement in the unaffected lungs. In all the AO areas, these combined images showed the matched perfusion and aerosol deposition defects. These images showed perfusion defects without aerosol deposition defects in the relatively small embolized areas, but showed the matched defects in the widely embolized areas probably due to hypoxic bronchial constriction. CONCLUSION: The combination MR studies may be acceptable for noninvasively defining regionally impaired lung function in AO and PE.     

Use of an optical flow method for the analysis of serial CT lung images

RATIONALE AND OBJECTIVES: Serial CT lung studies are difficult to compare due to misregistration between image sets. An optical flow method (OFM) was adapted for use on CT lung images to register images and visualize changes between studies. Three applications were investigated: lung nodule assessment; evaluation of pulmonary enhancement; and functional changes due to air trapping. MATERIALS AND METHODS: From an initial clinical study, a follow-up study was created by digitally manipulating the images to simulate patient positioning errors and nodule growth. Nodule growth was measured from the temporal subtraction of registered images. In application to the assessment of pulmonary enhancement, pre and postcontrast images from a patient with acute pulmonary embolism (PE) were registered. A map of the perfused blood volume was computed from the ratio of aligned lung volumes. Functional changes in the lung were demonstrated using images from a patient with air trapping. End-inspiratory and end-expiratory volumes were aligned and displacement fields estimated using the OFM. Principal strains were computed from the displacement fields. RESULTS: All image volumes were aligned with at least 0.95 correlation. OFM estimates of displacement showed excellent agreement with the prescribed displacements with 0.33 pixel RMS error. Nodule growth was evident in the presence of significant positioning errors. In the PE case, enhancement ratios indicated a hypoperfused area consistent with an occlusive hypodense filling defect. For the air trapping case, a strain map showed functional changes along the interface of the air trap. CONCLUSIONS: The OFM can facilitate the detection and quantification of changes between serial CT lung studies.     

山莨菪碱对海水淹溺兔外周血单核细胞NF-κB表达的干预作用

目的：探讨山莨菪碱对海水淹溺后兔外周血中单核细胞核转录因子κB（NF-κB）的表达以及海水淹溺性肺水肿（PE-SVCD）治疗作用。方法：家兔气管切开后模拟海水淹溺造成急性肺损伤,于淹溺前（T1）,淹溺后15、30、60、120、240、480min（T2～T7）7个时间点采集外周血进行血气分析,并测定外周血炎症介质含量和单核细胞中NF-κB的淹溺前后表达变化,并采集肺组织。结果：海水淹溺致兔急性肺损伤各时间点肺组织中性粒细胞大量浸润,淹溺后外周血单核细胞NF-κB的表达开始增高,90 min后达到最高峰,而山莨菪碱可降低NF-κB以及炎症因子表达（P〈0.01）。结论：海水淹溺急性肺损伤可能与NF-κB高表达有关。山莨菪碱可降低NF-κB表达,减轻肺损伤程度。     

高原昏迷12例的临床病理学研究

报道12例高原昏迷的病理组织学和超微结构变化,总结了本病的临床病理学特点并探讨其发病机理.脑重量1260～1730克,平均1448克。光镜观察脑组织疏松水肿,4例脑出血,6例小血管水肿并微血栓形成。神经细胞呈缺血缺氧性改变。电镜观察神经原纤维溶解,突触肿胀,髓鞘变性或解离,核蛋白体减少.本病基本原因为高原急性缺氧造成神经组织损伤和功能障碍,临床早诊断早治疗尤为重要.