低浓度臭氧暴露对哮喘大鼠气道炎症的影响

目的　以实验研究佐证流行病学调查发现的环境因素与哮喘发病率升高之间的关系 ,探讨低浓度臭氧暴露对哮喘敏感个体气道炎症的影响。方法SD大鼠 4 0只 ,随机分为 4组 ,即正常对照组 (N)、正常暴露组 (N0 .2 5)、哮喘组 (A)和哮喘暴露组 (A0 .2 5)。N0 .2 5组和A0 .2 5组进行O3暴露 ,O3暴露浓度为 0 .2 5mg·m- 3,N组和A组进行过滤空气暴露 ,各实验组均为急性 1次暴露 ,暴露时间为 3h ,暴露结束后 4h收集支气管 肺泡灌洗液 (BALF)进行指标测定。结果　①A0 .2 5组与N组和A组比较 ,BALF中细胞分类均有显著改变 (P <0 .0 1) ,A组大鼠BALF炎症细胞以嗜酸性细胞增加为主 ,N0 .2 5以非嗜酸性细胞增加为主 ,而A0 .2 5组嗜酸性细胞和中性粒细胞均有显著增加 ,呈混合浸润型。②各实验组大鼠BALF中NO水平与N组比较均有显著增加 (P <0 .0 1或P <0 .0 5 ) ,A0 .2 5组显著高于N0 .2 5组 (P <0 .0 5 ) ,但不高于A组 (P <0 .0 5 )。③A组IL 2显著高于N组(P <0 .0 1) ;N0 .2 5组IL 2和IL 6显著高于N组 (P <0 .0 1) ;A0 .2 5组IL 2 ,IL 6和IL 8均显著高于N组 ,N0 .2 5组和A组 (P <0 .0 1或P <0 .0 5 )。结论　低浓度O3急性暴露可加重哮喘大鼠变应性气道炎症反应 ,与其他炎症反应一样 ,IL 2 ,IL 6和IL 8等细胞因子在O3介     

一氧化氮与哮喘气道炎症实验研究

目的　评价一氧化氮 (Nitric Oxide,NO)在哮喘气道炎症防治中的作用。方法　用两种免疫学方法 (酶联免疫吸附试验和免疫组化 ABC方法 )和生理学方法测定了哮喘组和正常对照组豚鼠血浆和肺泡灌洗液 (BAL F)中 NO水平和肺组织上皮细胞中NOS(一氧化氮合成酶 )、ICAM- 1 (细胞间粘附分子 - 1 )表达及肺功能改变。结果　与对照组比 ,1哮喘豚鼠血浆可溶性 ICAM- 1水平上升 ,BAL F中 NO水平上升 (P<0 .0 5 ) ;2肺组织 NOS、ICAM- 1表达水平上调 (P<0 .0 5 ) ;3肺潮气量和动态肺顺应性下降 ,气道阻力上升 (P<0 .0 5 )。结论　NO介导了哮喘气道炎症     

罗红霉素通过诱导型一氧化氮合酶/一氧化氮途径抑制哮喘大鼠气道炎症

目的探讨罗红霉素对哮喘大鼠支气管诱导型一氧化氮合酶(iNOS)及一氧化氮(NO)的影响。方法24只成年哮喘大鼠随机分成对照组、哮喘组以及罗红霉素组。对支气管肺泡灌洗液(BALF)细胞总数及嗜酸性粒细胞计数,免疫组织化学检测大鼠支气管上皮细胞iNOS蛋白表达,RT-PCR检测肺组织iNOS mRNA表达,分光光度计检测肺组织iNOS活性及NO含量。双抗体夹心法检测肺组织白细胞介素-4(IL-4)及干扰素-γ(IFN-γ)。结果哮喘组大鼠BALF细胞总数及嗜酸性粒细胞分类分别为(7.28±1.65)×108.L-1、(7.73±1.54)%,均高于对照组(3.76±0.97)×108.L-1、(1.27±0.60)%;罗红霉素组BALF细胞总数及嗜酸性粒细胞分类分别为(5.68±0.95)×108.L-1、(5.54±1.53)%,明显低于哮喘组,差异有统计学意义。哮喘组肺组织IL-4浓度、iNOS活性及NO含量高于对照组,罗红霉素组肺组织IL-4浓度、iNOS活性及NO含量低于哮喘组。哮喘组肺组织IFN-γ浓度低于对照组,罗红霉素组肺组织IFN-γ浓度高于哮喘组。哮喘大鼠支气管上皮细胞iNOS蛋白及肺组织iN-OSmRNA表达分布吸光度值分别为(0.25±0.06)、(0.52±0.14),较对照组[(0.14±0.05),(0.33±0.05)]明显增强;但罗红霉素组iNOS蛋白及mRNA表达为(0.15±0.03)、(0.35±0.07),均明显较哮喘组减弱。结论罗红霉素通过干预哮喘大鼠气道IL-4、IFN-γ以及iNOS/NO体系,抑制哮喘气道炎症反应。     

强的松对哮喘小鼠气道T淋巴细胞炎症的影响

目的：研究强的松对小鼠气道T淋巴细胞炎症的影响。方法：卵蛋白致敏及激发制成小鼠哮喘模型。免疫组化方法测定强的松对气道T淋巴细胞亚群的影响。结果：哮喘小鼠气道组织CD25^ 、CD4^ 、CD8^ 细胞的数目较正常对照组明显增多；哮喘小鼠应用强的松后气道组织CD25^ 、CD4^ 、CD8^ 细胞的数目较哮喘组明显减少。结论：1、哮喘小鼠气道组织存在T淋巴细胞的活化加强及浸润。2、小剂量强的松能抑制哮喘小鼠气道T淋巴细胞活化及浸润。     

阿托伐他汀对哮喘大鼠气道炎症及气道重构的影响

目的：探讨阿托伐他汀对卵清白蛋白致敏哮喘模型大鼠气道炎症和重构的影响。方法清洁级 SD 雄性大鼠24只按随机数字表法分为对照组、哮喘组和阿托伐他汀组,每组8只。对照组大鼠采用0．9％氯化钠溶液（生理盐水）进行致敏和激发,哮喘组大鼠采用卵清白蛋白致敏和激发,阿托伐他汀组在致敏和激发前以阿托伐他汀口服。采用肺功能检测3组大鼠气道呼气阻力;采用图像分析软件测定肺组织切片中的支气管壁内周长、支气管管壁面积、支气管平滑肌面积;胶原表达通过气道壁 Masson 染色进行观察;实验动物血清中白介素－13（IL－13）及转化生长因子－β1（TGF－β1）的水平以 ELISA 法测定。结果肺功能检测显示哮喘组平均呼气阻力显著升高,阿托伐他汀组低于哮喘模型组（ P ＜0．05）;病理检查显示哮喘组气道炎症明显,对照组和阿托伐他汀组与之相比炎症轻微;阿托伐他汀组大鼠气道管壁面积、平滑肌面积图像分析和哮喘组比较差异有统计学意义（ P ＜0．05）;阿托伐他汀组肺组织中胶原沉积表达较哮喘组减少（ P ＜0．05）;阿托伐他汀组大鼠血清中 IL－13和 TGF－β1较哮喘组降低（ P ＜0．05）。结论阿托伐他汀能够明显减轻哮喘大鼠气道炎症,降低哮喘大鼠的气道基本阻力;减少肺组织中胶原沉积,降低气道管壁面积、平滑肌层面积,减轻哮喘气道重构。阿托伐他汀治疗能够降低血清中 TGF －β1和 IL－13水平,或为其减轻炎症和气道重构的机制。     

咪喹莫特抑制哮喘大鼠气道炎症转录水平的研究

目的：探讨咪喹莫特拮抗支气管哮喘气道炎症的分子机制。方法：卵清蛋白腹腔注射与雾化吸入建立大鼠哮喘模型，采用逆转录－聚合酶链反应（RT－PCR）测定了不同剂量咪喹莫特对哮喘大鼠肺组织白介素（IL）－4mRNA、IL－5mRNA、IL－12mRNA和干扰素（IFN）－γ mRNA表达的影响。结果：咪喹莫特各治疗组及地塞米松组能显抑制哮喘大鼠肺组织中IL－4、IL－5mRNA的表达（与哮喘相比，均为P＜0．001；与空白对照组比，均为P＞0．05），各咪喹莫特组同时能显增加IL－12、IFN－γ mRNA表达（与哮喘组比，均为P＜0．001；与空白对照组比，均为P＞0．05），而地塞米松组不能增加IL－12、IFN－γ mRNA的表达（与哮喘组比，均为P＞0．05；与空白对照组比，均为P＜0．001）。咪喹莫特各治疗组间无显性差异。结论：咪喹莫特能降低哮喘大鼠肺组织中IL－4和IL－5基因转录，增加IL－12和IFN－γ基因转录，进而 抑制嗜酸性粒细胞的聚集、活化，发挥其抗气道炎症的作用。     

舒利迭雾化吸入对哮喘小鼠气道炎症及气道重构的影响

目的 研究舒利迭雾化吸入对哮喘小鼠炎症及气道重构的影响.方法 将30只雄性小鼠随机分成卵白蛋自(OVA)致敏致哮喘组(A组)、舒利迭干预组(B组)、正常对照组(C组).用OVA进行致敏和激发,建立哮喘模型.收集小鼠支气管肺泡灌洗液(BALF)行白细胞和嗜酸粒细胞(EOS)计数,采用医学图像分析软件测定支气管各项指标;HE染色观察组织形态学变化.结果 正常对照组、哮喘组、舒利迭干预组的EOS分别是(0.54±0.16)、(6.82±0.5 7)、(3.19±0.66)×10<'5>/m1,A组气道壁炎性细胞计数、气道平滑肌面积、气道内壁面积均明显高于C组,两组比较差异有统计学意义(P<0.01),B组各项指标均明显低于A组,差异有统计学意义(P<0.01),B组与C组比较各项均有升高,差异有统计学意义(P<0.01,P<0.05).结论 舒利迭雾化吸入不仅可明显抑制哮喘小鼠的气道炎症反应,还可明显减轻气道重构的程度.     

罗红霉素对哮喘大鼠气道炎症及气道高反应性的影响

目的 观察罗红霉素对哮喘大鼠气道炎症、气道高反应性的影响。方法 30只雄性SD大鼠随机分组和建模,罗红霉素干预28天,检测气道反应性和支气管肺泡灌洗液中的IL-4、IL-5、IFN-γ。结果 罗红霉素组气道反应性以及BALF中IL-4、IL-5低于哮喘组。有显著性差异;结论 罗红霉素具有减轻哮喘大鼠气道炎症和气道反应性。     

老年人支气管哮喘呼出气一氧化氮与气道炎症的关系

目的 分析老年人支气管哮喘呼出气一氧化氮(FeNO)与气道炎症的相关性.方法 选取2019年1月至2021年1月门诊接诊的60例老年支气管哮喘患者作为观察组,以及同期门诊体检的60例健康人员作为参照组,检测、比较2组FeNO、气道炎症参数,比较不同程度哮喘患者FeNO、气道炎症参数,比较急性发作、非急性发作组FeNO、...     

玉簪花提取物对RAW264.7细胞炎症及哮喘小鼠气道炎症的影响

目的 研究玉簪花提取物对RAW264.7巨噬细胞炎症模型和BALB/c小鼠支气管哮喘模型的影响。方法 建立脂多糖与人干扰素-γ诱导的RAW264.7细胞炎症模型,用玉簪花提取物预处理模型细胞,测定细胞上清液中一氧化氮(NO)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)的水平。将BALB/c小鼠随机分为空白组、模型组、阳性组、玉簪花提取物高、低剂量组。采用卵清蛋白致敏和激发哮喘,末次给药24 h后,分析小鼠全血中淋巴细胞、单核细胞、粒细胞的数量,吉姆萨染色观察嗜酸性粒细胞的数目;ELISA法检测小鼠血清中总免疫球蛋白E(IgE)的水平、NO的含量、支气管肺泡灌洗液中IL-6与TNF-α的水平以及肺组织细胞黏附因子-1(ICAM-1)的水平;HE染色观察小鼠肺组织炎症及病理变化。结果 玉簪花提取物可显著抑制炎症细胞因子的表达;显著降低卵清蛋白模小鼠炎症细胞和嗜酸粒的数量,减少NO生成,降低IgE的含量,显著降低肺泡灌洗液中IL-6、TNF-α的水平以及肺组织中ICAM-1的表达。结论 玉簪花提取物对细胞炎症模型和哮喘气道炎症模型有较好的抑制作用,可为其治疗哮喘的研究提供参考。     

哮喘患者不同 FeNO 水平与哮喘炎症表型的关系研究

目的：探讨支气管哮喘患者的呼出气一氧化氮（ FeNO）水平变化与患者炎症表型的关系。方法选取呼吸内科收治的支气管哮喘患者100例（哮喘组）和门诊体检健康研究对象100例（健康组）,分别检测2组对象的FeNO水平及血清炎症因子等指标并进行比较分析。结果哮喘组患者的ECP、IL－2、IL－4、IL－6、IL－8、IL－13、TNF－α、IFN－γ、FeNO测定值均显著的高于健康组（ P ＜0．05）,哮喘组患者的IL－2、IFN－γ测定值均显著的低于健康组（ P ＜00．5）;急性发作期哮喘组患者的ECP、IL－2、IL－4、IL－6、IL－8、IL－13、TNF－α、IFN－γ、FeNO测定值均显著的高于缓解期哮喘患者（ P ＜0．05）,急性发作期哮喘组患者的IL－2、IFN－γ测定值均显著的低于缓解期哮喘患者（ P ＜0．05）;哮喘组患者的ECP、IL－2、IL－4、IL－6、IL－8、IL－13、TNF－α、IFN－γ与FeNO测定值呈显著的正相关关系（ P ＜0．05）,哮喘组患者的IL－2、IFN－γ测定值与FeNO测定值呈显著的负相关关系（ P＜0．05）。结论支气管哮喘患者的FeNO水平、炎症指标均显著的升高,FeNO水平与哮喘患者的病情及炎症反应程度具有显著的正相关关系。     

Exposure to ozone induces a systemic inflammatory response: possible source of the neurological alterations induced by this gas

Abstract

The World Health Organization identified urban outdoor air pollution as the eighth highest mortality risk factor in high-income countries. Exposure to ambient pollutants such as ozone (O₃) increases the number of hospital admissions. O₃ is a highly reactive gas that reacts with cells lining the airways, producing the formation of reactive oxygen species and inflammation. Beyond the respiratory system, O₃ exposure also produces fatigue, lethargy, headaches, and significant decrease in rapid-eye-movement sleep related to an increase in slow-wave sleep. Interestingly, these sleep changes can be significantly mitigated by treatment with indomethacin, which suggests that an inflammatory mechanism may be responsible for these neurological symptoms. To characterize the inflammatory mechanisms by which O₃ affects tissues outside the pulmonary system, we evaluated inflammatory factors in both lung and brain. Rats exposed to 1 part per million O₃ for 1, 3 or 6?h, as well as rats exposed daily for 1 or 3?h over five consecutive days, showed increases in TNF-α and IL-6 levels within the lungs as well as increases in TNF-α, IL-6, NF-κB p50 and GFAP levels in the cerebral cortex. These results support the hypothesis that the neuroinflammatory response may be responsible for the central nervous system effects of O₃ exposure.     

Relationship of pulmonary function response to ozone exposure and capsaicin cough sensitivity

Abstract

Context: Challenge studies in humans have shown considerable interindividual variability in pulmonary impairment across ozone exposure.

Objective: Since previous results suggested effect modulation by neural mechanism, we investigated sensory C-fiber reactivity in relationship to ozone-triggered response pattern.

Methods: Cough reflex thresholds reflecting C-fiber sensitivity were evaluated by capsaicin single breath dose–response method. Capsaicin concentrations triggering, respectively, two and five or more coughs (C2, C5) were recorded. Sixteen healthy subjects were randomly exposed in an intermittent exercise protocol to ozone concentrations of 240 and 40?ppb (sham exposure). Ozone responsiveness was defined by a decrease in forced expiratory volume in 1?s (FEV₁) of more than 5%.

Results: Based on a dichotomous classification, subjects with enhanced reactivity to ozone had lower cough thresholds than non-responders (C2, p?=?0.035; C5, p?=?0.086). Over all, we could demonstrate relationships between capsaicin sensitivity and ozone-triggered changes in FEV₁, peak expiratory flow and maximal expiratory flow at 50% vital capacity but not in specific airway resistance.

Conclusion: Our results suggest that capsaicin challenge tests might be useful to characterize subjects with enhanced pulmonary function response towards inhalant irritants.     

Enhancement of nasal inflammatory and epithelial responses after ozone and allergen coexposure in Brown Norway rats.

Repeated exposures to ozone cause inflammation and mucous cell metaplasia (MCM) in the nasal mucosa of laboratory animals. Similar cellular responses occur in humans during allergic rhinitis. We tested the hypothesis that exposure to ozone will enhance the inflammatory and epithelial responses associated with allergic rhinitis. Ovalbumin (OVA)-sensitized Brown Norway rats were exposed to ozone (0.5 ppm, 8 h/day) for 1 day or 3 consecutive days. Immediately after each ozone exposure, animals were challenged intranasally (IN) with either sterile saline or OVA dissolved in saline (1%, 50 microg/nasal passage). Twenty-four h after the last IN challenge rats were sacrificed; nasal tissues were removed and processed for light microscopic examination and morphometric analysis of numeric densities of inflammatory and epithelial cell populations and volume densities of intraepithelial mucosubstances. A single OVA challenge caused a significant influx of neutrophils and eosinophils into the submucosa of all nasal tissues. Ozone exposure further enhanced the appearance of eosinophils in the maxilloturbinates of OVA-challenged rats but did not increase inflammation in other nasal tissues. After 3 days of ozone/OVA coexposures, the nasal transitional epithelium lining the maxilloturbinates had increased numbers of epithelial cells as well as the appearance of mucus-containing cells in areas normally absent of these secretory cells (i.e., MCM). Multiple challenges with OVA caused increased epithelial mucosubstances in the respiratory epithelium lining the septum without increasing the number of epithelial cells. Multiple exposures to both ozone and OVA caused greater increases in intraepithelial mucosubstances in the septum than those elicited by OVA alone. These results demonstrate that exposure to ozone exacerbates epithelial and inflammatory responses associated with allergen challenge. In addition, coexposure of these agents enhanced the induced production of nasal mucosubstances caused by either agent alone.     

Ovalbumin-Induced Airway Inflammation and Fibrosis in Mice Also Exposed to Ozone

A murine model of allergen-induced airway inflammation was used to examine the effects of exposure to ozone on airway inflammation and remodeling. Sensitized BALB/c mice were exposed to ovalbumin aerosol for 4 wk before and after 2 wk of exposure to either 0.2 ppm or 0.5 ppm ozone. Other groups of mice were exposed to ovalbumin aerosol for 6 wk with continuous concurrent exposure to ozone during wk 1–6, or during intermittent concurrent exposure to ozone. Lung inflammation was measured by quantitative differential evaluation of lung lavage cells and by histological evaluation of stained lung sections. Alterations in lung structure (airway fibrosis) were evaluated by quantitative biochemical analysis of microdissected airways. The same total number of cells was observed in lavage fluid from animals exposed for 4 wk to ovalbumin alone or to ovalbumin for 4 wk immediately before or after exposure to 2 wk of 0.2 or 0.5 ppm ozone. Mice exposed to ovalbumin for 6 wk with concurrent exposure to either 0.2 ppm or 0.5 ppm ozone during wk 3–6 had a significant decrease in the total number of cells recovered by lavage. Values as low as 7% of the cell number found in mice exposed to ovalbumin aerosol alone were observed in the mice exposed to ovalbumin plus 0.2 ppm ozone during wk 3–6. There were significant differences in the cell differential counts in the lavage fluid from mice exposed to ovalbumin alone as compared with values from mice exposed to ovalbumin and ozone under all of the protocols studied. When ozone was given for 2 wk prior to ovalbumin exposure (Experiment 1), there were a high percentage of macrophages and low percentages of lymphocytes and eosinophils in the lung lavage. When ozone was given for 2 wk after ovalbumin exposure (Experiment 2), there were a moderate percentage of macrophages, a low percentage of eosinophils, and a high percentage of lymphocytes in the lung lavage. When ozone and ovalbumin were given simultaneously (Experiments 3 and 4), there were a high percentage of macrophages in the lavage with 0.2 ppm ozone and a high percentage of eosinophils. Ozone appears to antagonize the specific inflammatory effects of ovalbumin exposure, especially when given before or during exposure to ovalbumin. Airway remodeling was examined by two different quantitative methods. None of the groups exposed concurrently to ovalbumin and ozone had a significant increase in airway collagen content as compared to the matched groups of mice exposed to ovalbumin alone. The findings were consistent with an additive response of mice to simultaneous exposure to ovalbumin and ozone. Ozone exposure alone for 6 wk did not affect the number of goblet cells in the airways, while mice exposed to ovalbumin aerosol alone for 6 wk had about 25% goblet cells in their conducting airways. Concurrent exposure to ovalbumin and 0.2 ppm ozone caused significant increases in goblet cells (to 43% of total cells) in the conducting airways of the exposed mice. We conclude that when mice with allergen-induced airway inflammation induced by ovalbumin are also exposed to ozone, the lung inflammatory response may be modified, but that this altered response is dependent on the sequence of exposure and the concentration of ozone to which they are exposed. At the concentrations of ozone tested, we did not see changes in airway fibrosis. However, goblet-cell hyperplasia appeared to be increased in mice exposed concurrently to ovalbumin and 0.2 ppm ozone.     

Impact of ozone on claudins and tight junctions in the lungs

Claudins (CLDNs) are a major transmembrane protein component of tight junctions (TJs) in endothelia and epithelia. CLDNs are not only essential for sustaining the role of TJs in cell permeability but are also vital for cell signaling through protein‐protein interactions. Ozone induces oxidative stress and lung inflammation in humans and experimental models, but the impact of ozone on claudins remains poorly understood. This study was to determine the expression of TJ proteins, such as claudin 3, 4, 5, and 14 following ozone exposure. Mice were exposed to 0.1, 1, or 2 ppm of ozone or ambient air for 6 h for 3 days. The impact of ozone on CLDNs, Nrf2, Keap1, and reactive oxygen species (ROS) were estimated using immunoblotting, immunohistochemical staining, confocal imaging, and ELISA analysis in mice and bronchial epithelial cells. Mice exposed to ozone experienced increased airway inflammatory cell infiltration and bronchial hyper‐responsiveness compared to control mice. Additionally, CLDN3, CLDN4, ROS, Nrf2, and Keap1 protein expression increased, and lung CLDN14 protein expression decreased, in mice exposed to ozone compared with control mice. These results indicate that CLDNs are involved in airway inflammation following ozone exposure, suggesting that ozone affects TJ proteins through oxidative mechanisms.     

射频热凝术结合臭氧治疗椎间盘源性腰痛的临床效果

目的 探讨射频热凝术联合臭氧治疗椎间盘源性腰痛患者的临床效果。 方法 收集 2013 年 10 月— 2015 年 10 月在我院采用射频热凝术联合臭氧治疗的 120 例腰椎间盘突出症患者的临床资料。 手术前后疼痛情况采用疼痛视觉模拟（VAS）评分（于患者术前和术后 1 周, 1、3、6、12 个月给予）, 健康调查简表（SF-36）评分（于患者术前及术后 6 个月给予）。 疗效评定采用改良 MacNab 标准。 结果 患者 VAS 评分术前为 7.02±0.64, 术后 1 周, 1、3、6、12 个月时分别为 3.13±0.32、2.11±0.67、2.62±0.89、2.37±0.34、2.31±0.50, 术后均较术前降低（P < 0.05）。 患者术前SF-36 评分为 48.32±7.46, 术后 6 个月（82.03±5.89）较术前增加（P < 0.05）。 术后 6 个月改良 MacNab 标准评定结果显示患者优良率为 89.17%。 结论 射频热凝术联合臭氧治疗椎间盘源性腰痛是一种有效、可靠的方法。     

Alveolar permeability to protein in rats differentially susceptible to ozone

Sprague-Dawley rats susceptible (DS) to NaCl-induced hypertension suffer higher mortality when exposed daily to 2.0 ppm ozone than do hypertension-resistant (DR) rats, independent of salt in the diet or systemic blood pressure. To investigate one possible contribution to this differential sensitivity to ozone, alveolar permeabilities to serum albumin were measured both in ozone-exposed and in control DS and DR rats. Female rats aged 5-7 weeks maintained on a low-salt (0.4% NaCl) diet were injected intravenously with 125I-bovine serum albumin and were then exposed to either 2.0 ppm ozone or air for 5 h. After pentobarbital anesthesia, the rats were exsanguinated and their lungs were lavaged in situ with saline. Lavage fluids and blood samples were measured for radioactivity using a NaI-well gamma counter. The results indicated that while DS and DR control rats have similar pulmonary permeabilities to 125I-albumin, the lungs of the ozone-exposed DS animals were 63% (p less than 0.02) more permeable than those of DR rats exposed to ozone. Sloughing of epithelial tissue, mucous formation and an accumulation of macrophages in the end-airways were more pronounced among ozone-exposed DS animals than in DR-ozone-exposed rats. This increased damage among DS rats correlated well with the increased protein permeability levels. In similar studies, Sprague-Dawley (D) rats were more variable in their response to ozone than either inbred strain. However, the results appeared generally more like those of the DS animals, suggesting that the trait selected by inbreeding may have been resistance rather than sensitivity to ozone-induced lung injury.