大鼠肺微血管和肺泡铸型的扫描电镜观察

用扫描电镜观察以甲基丙烯酸甲酯灌注鼠的肺微血管和肺泡。胸膜下毛细血管较稀疏,网孔粗大。毛细血管部分成锐角折返,亦可见毛细血管盲端。肺泡隔毛细血管均成扁平状膨大,且相互吻合成单层密集网。肺泡铸型为大小不等、不规则的多面体,表面可见肺泡Ⅱ型细胞核之压迹。两肺泡之间可见呈桥式连接的肺泡孔,亦可见部分呈三通管样相连。     

糖尿病酮症酸中毒家兔肺泡超微结构和细胞化学的研究

目的:研究糖尿病酮症酸中毒肺损伤的发病机制。方法:实验组(DK组,n=6)给予四氧嘧啶(alloxen)150 mg.kg-1和链脲佐菌素(STZ)150 mg.kg-1,对照组(NS组,n=6)使用生理盐水,72 h后行动脉血气分析,处死动物,取肺组织标本,做病理学检查,采用铅离子捕获法做常规超微结构、酸性磷酸酶(ACPase)细胞化学检查。结果:NS组血气分析正常;肺泡上皮细胞组织结构完整;溶酶体内ACPase活性表达,溶酶体结构完整。DK组体质量下降,动脉血气分析显示达到糖尿病酮症酸中毒标准;光镜可见肺泡内出血和肺泡隔的增厚、断裂;超微结构可见有肺泡上皮损伤、血管内有炎症细胞贴壁、肺泡内见炎症细胞等改变;肺泡上皮细胞内溶酶体形态不规则,细胞浆内有散在黑色酶颗粒,溶酶体数量增多。结论:糖尿病酮症酸中毒能引起肺上皮细胞组织结构损坏和细胞内溶酶体的破坏。     

大鼠DDVP中毒急性肺损伤模型的建立

【目的】建立敌敌畏(DDVP)中毒大鼠急性肺损伤(acute lung injury,ALI)的实验动物模型。【方法】健康Wistar雄性大鼠36只,随机分为对照组和染毒组2组,每组18只。采取腹腔注射累积给药法,检测给药前后各组的动脉血气分析、血浆SOD+MDA的变化及肺组织病理学改变。【结果】染毒组动物均出现口唇及四肢紫绀、惊厥,测动脉血气符合ALI。ALI发生后,PaO2及SaO2明显下降;氧合指数(PaO2/FiO2)均<300。发生ALI时,染毒组大鼠的SOD水平均较给药前下降;而MDA水平均较给药前升高。染毒组大鼠肺组织HE染色可见肺泡间隔增厚,肺泡壁毛细血管壁充血、灶状出血,部分肺泡水肿及炎性细胞浸润。【结论】本实验成功模拟了DDVP中毒所致ALI的模型,且该模型稳定、重复性好。     

淡水淹溺大鼠肺表面活性物质相关蛋白质A表达变化的研究

目的观察淹溺后大鼠呼吸、血气、病理及肺表面活性物质相关蛋白质A(SP-A)的变化特点。方法将24只健康雄性大鼠随机分为对照组(6只)和淹溺组(18只),再将淹溺组分为淹溺后2h组、淹溺后4h组和淹溺后6h组,每个亚组6只大鼠。于上述时间点记录大鼠的呼吸频率,经颈动脉采血测血气。处死大鼠后取肺组织行HE染色,观察淹溺后肺组织普通病理变化,采用免疫组织化学法检测SP-A在灌注后不同时间点的变化。结果淹溺组大鼠淡水灌注后呼吸先增快,以后逐渐减慢,但未降至正常范围。PaO2在灌入淡水后5min显著下降[(48.7±3.93)mmHg比(93.65±6.02)mmHg,P<0.05],之后虽有回升,但维持在较低水平。PaCO2在灌入淡水后5min显著上升[(36.20±4.41)mmHg比(55.96±4.60)mmHg,P<0.05],随后降低,显著低于正常水平(P<0.05)。对照组大鼠SP-A主要以膜状形式连续分布于肺泡腔表面。淹溺组大鼠肺泡壁有不同程度的断裂,肺泡腔内可见红细胞聚集,间质水肿明显,呈局灶性肺不张,SP-A主要以颗粒状聚集在肺泡腔内表面和渗液表面,SP-A表达量较对照组显著降低(P<0.05)且进行性下降。结论淡水淹溺后造成肺损伤,导致SP-A的质和量发生改变。     

茶尘对大鼠肺部损害的光镜和电镜观察

用光镜和电镜对自然吸入茶尘的大鼠肺进行观察。可见茶尘在肺内沉着,形成气道炎、肺泡炎、间质肉芽肿、轻度纤维增生和较重的肺气肿。网状纤维增生发生于染尘后第6个月,胶原纤维增生发生于第9个月。Ⅰ型肺泡上皮细胞变性、坏死、数量减少。Ⅱ型细胞增多。肺泡隔增厚、毛细血管周围纤维母细胞和胶原纤维均有增生,提示茶尘可引起肺组织改变和损害。     

急性高原缺氧大鼠肺组织损伤及其机制研究

【目的】通过建立低压缺氧模型,模拟急性高原缺氧损伤,观察不同缺氧时间点大鼠肺组织损伤情况。【方法】选取清洁级雌性SD大鼠60只,随机分为正常对照组、缺氧6、12及24 h组。利用数控低压缺氧舱,建立急性高原缺氧损伤模型,通过HE染色观察大鼠肺组织形态学改变,利用干湿比重法检测肺组织含水量,采用生化手段检测血清乳酸脱氢酶(lactatedehydrogenase,LDH)及过氧化氢酶(catalase,CAT)活性,应用Western blotting技术检测肺组织水通道蛋白(aquaporin,AQP)1/4的表达情况。【结果】HE染色:正常对照组可见多边形或圆形薄壁囊泡,边界清楚,肺泡上皮细胞间为薄壁肺泡隔,隔内可见毛细血管断面,各低压缺氧组肺泡上皮细胞明显肿大,肺泡壁增厚,肺间隔内毛细血管扩张;与正常对照组相比,各缺氧组大鼠肺含水量显著升高(P<0.01),且随缺氧时间的延长而逐渐增高;与正常对照组相比,各缺氧组大鼠血清LDH活性显著升高(P<0.01),CAT活性显著下降(P<0.05或P<0.01);与正常对照组相比,各缺氧组大鼠肺组织中AQP1/4蛋白表达量均明显升高(P<0.01),且随缺氧时间的延长而逐渐增高。【结论】急性高原缺氧可造成实验大鼠肺水肿,且损伤程度与缺氧时间密切相关,其机制可能为上调水通道蛋白(AQP)1/4的表达所致。     

产前用地塞米松对鼠肺泡形态发育的影响

目的探讨孕期肌注地塞米松对新生大鼠肺泡形态发育的影响.方法 16只SD孕大鼠分为对照组和观察组,每组8只,分别于孕18、19、20d肌注9g/L氯化钠溶液0.5ml和地塞米松0.8mg·kg-1·d-1,以9g/L氯化钠溶液稀释至0.5ml,足月自然分娩后取新生4、10、14日龄大鼠肺组织,病理切片,HE染色,观察肺泡形态学的改变,进行计算机图像分析.结果同日龄新生大鼠比较,观察组肺泡间隔厚度、肺泡表面积/肺泡体积、肺泡数、次级隔高、次级隔数均低于对照组(均P＜0.01),肺泡面积大于对照组(P＜0.01).结论孕期肌注地塞米松可影响新生鼠肺泡形态发育,使呼吸膜面积减小,阻碍肺泡化.     

骨髓间充质干细胞移植对大鼠急性肺水肿病理学影响

目的:探讨骨髓间充质干细胞移植对SD大鼠急性肺水肿模型的病理学影响。方法:将80只大鼠随机分为肺水肿组、干细胞治疗组、干细胞预防组、空白对照组、干细胞对照组5组,每组16只。对SD大鼠腹腔注射6%NH4Cl建立急性肺水肿模型,预防组、治疗组分别于肺水肿模型建立前后30min移植干细胞,移植后不同时间(30min,2h,1d,7d)活杀SD大鼠取肺脏,固定后用常规光镜及扫描电镜观察大鼠肺脏病理学变化。结果:肺水肿模型大鼠30min肺泡结构基本正常,2h时肺泡腔内可见大量渗出物,肺泡壁毛细血管明显充血。7d时部分肺泡壁增厚。干细胞治疗组大鼠30min肺组织结构基本正常,2h时部分区域肺泡腔内可见少许渗出物。7d时肺组织结构基本正常。干细胞预防性移植大鼠的肺组织在30min,2h,1d,7d病理学改变基本同肺水肿模型大鼠。结论:腹腔注射氯化铵可建立急性肺水肿模型,骨髓间充质干细胞治疗性移植可减轻急性肺水肿病理学改变,而骨髓间充质干细胞预防性移植不能减轻急性肺水肿病理学改变。     

肺铸型的扫描电子显微镜观察

本文用扫描电镜观察了ABS丁酮液灌注的大鼠肺及其毛细血管的立体构筑。结果表明,肺泡铸型表面光滑,大小不等,肺泡间有桥形的肺泡孔相连,肺泡表面有肺泡Ⅱ型细胞顶端的压迹。肺血管铸型可见具有内皮细胞纵向压迹的小动脉和直径小于100μm的中间小动脉,毛细血管的网眼小于其本身的直径。作者对上述现象联系肺功能进行了讨论。     

骨髓间充质干细胞对肺损伤大鼠的治疗作用

目的:观察骨髓间充质干细胞(MSCs)对大鼠肺损伤的治疗作用.方法:将SD大鼠MSCs用DAPI标记后注入受体大鼠体内.将受体大鼠分为4组:肺损伤组、MSCs治疗组、MSCs对照组和正常对照组.2 wk后观察肺组织结构、植入细胞的变化,同时检测支气管肺泡灌洗液中层黏连蛋白、透明质酸以及肺组织羟脯氨酸含量的变化.结果:MSCs治疗组大鼠肺组织中可见少量DAPI标记的细胞,其中部分细胞表达广谱细胞角蛋白,肺间质增生减轻;支气管肺泡灌洗液中层黏连蛋白、透明质酸及肺组织羟脯氨酸的含量在肺损伤组均有明显升高(P＜0.01),而在MSCs治疗组均有所下降(P＜0.01).结论:MSCs可在损伤的大鼠肺组织中分化为肺泡上皮细胞,降低支气管肺泡灌洗液中层黏连蛋白、透明质酸及肺组织羟脯氨酸的含量,减轻大鼠肺损伤及纤维化的形成.     

K252a对内毒素诱导急性肺损伤大鼠的保护作用

目的观察K252a（MLK3阻断剂）对内毒素性急性肺损伤大鼠肺病理组织学改变及生存率的影响。方法采用尾静脉注射脂多糖（1ipopolysacharide,LPS）复制内毒素性急性肺损伤模型。90只大鼠随机分为6组（n=15）：对照组（control组）、LPS组、K252a50μg/kg组（K50组）、K252a75μg／kg组（K75组）、K252a100μg/kg组（K100组）和溶剂对照组（DMSO组）。模型制备成功后6h取肺脏进行光镜检查,观察48h内大鼠死亡情况并比较累计生存率。结果48h内LPS组、K50组、K75组和K100组以及DMSO组大鼠生存率分别为6．3％、27％、72％、57％及6．7％。光镜下可见LPS组大鼠肺组织结构明显被破坏,主要表现为肺泡内出血、肺问质水肿、肺泡萎陷以及肺组织内大量炎性细胞浸润。与LPS组相比,预先应用K252a组肺组织的损伤程度较轻微、肺间隔轻度增宽、无明显出血、少量炎性细胞浸润,尤其K75组,减轻程度最明显。结论K252a延迟LPS大鼠死亡时间,并呈现剂量依赖性,75μg/kgK252a剂量可以明显提高其生存率。并可改善内毒素性急性肺损伤大鼠肺脏的病理组织学结果。     

肺冲击伤的病理组织学和超微结构变化

用200g TNT炸药在模拟激波管内爆炸,使管口处的14只狗、12只豚鼠和20只大鼠造成不同程度的冲击伤。伤后6～8h活杀,作肺的大体、光镜和电镜观察。除见有典型的肺出血和肺水肿外,电镜下见肺上皮细胞和毛细血管内皮细胞肿胀和细胞器变性,内皮细胞变化更为严重。毛细血管腔内有中性白细胞和血小板积聚、附壁和脱颗粒等表现,对其意义作了讨论。     

大鼠油酸性急性肺损伤初期水通道蛋白4在肺水代谢的实验研究

目的 测定油酸造成急性肺损伤(ALI)初期损伤程度及肺泡Ⅱ型上皮细胞(ATⅡ)上水通道蛋白4(AQP-4)的表达量以评估病理状态下ATⅡ细胞水通道水转运能力的状况.方法 血气分析、观察肺组织病理学、用重力法测定血管外肺水(EVLW)含量检测早期肺损伤的程度;急性分离纯化大鼠油酸ALI模型的ATⅡ细胞,显微镜及电子显微镜观察形态病理变化:免疫组化了解肺组织AQP-4的表达,采用逆转录-聚合酶链反应(RT-PCR)检测肺泡Ⅱ型上皮细胞AQP-4的m-RNA表达的情况.结果 血气分析、光镜下肺损伤评分及EVLW油酸组严重程度显著高于对照组,显微镜下肺泡Ⅱ型上皮细胞的数量较对照组无明显减少,但电镜下细胞的超微结构改变,板层小体排空,线粒体损伤等改变;肺组织免疫组化观察到AQP-4明显表达增强,肺泡Ⅱ型上皮细胞AQP-4的m-RNA表达增多,AQP-4由胞浆向胞膜转运,胞膜的表达增多(P<0.05).结论 在肺损伤初期就有了肺损伤水肿的病理生理的改变,AQP-4在肺泡Ⅱ型上皮细胞上m-RNA及细胞膜的表达上调.很大程度调节肺泡腔及肺泡上皮细胞的水转运,在钠通道功能下降的情况下发挥了重要的代偿作用.     

Protective Effect of Tanshinone Ⅱ A on Lipopolysaccharide-induced Lung Injury in Rats

Objective:To explore the protective effect of tanshinoneⅡA on lipopolysaccharide(LPS)-induced lung injury in rats,and possible mechanism.Methods:LPS(O111:B4) was used to produce a rat model of acute lung injury.Sprague-Dawley rats were randomly divided into 3 groups(8 in each group):the control group,the model group(ALI group),and the tanshinoneⅡA treatment group.Expression of adhesion molecule CD18 on the surface of polymorphonuclear neutrophil(PMN-CD18) in venous white blood cells(WBC),and changes in coagulation-anticoagulant indexes were measured 6 h after injection of LPS or normal saline.Changes in malondialdehyde(MDA) content,wet and dry weight(W/D) ratio and morphometry of pulmonary tissue as well as PMN sequestration in the lung were also measured.Results:(1) When compared with the control group,expression of PMN-CD18 and MDA content were enhanced in the ALI group with a hypercoagulable state(all P<0.01) and an increased W/D ratio(P<0.05).Histopathological morphometry in the lung tissue showed higher PMN sequestration,wider alveolar septa;and lower alveolar volume density(VV) and alveolar surface density(SV),showing signif icant difference(P<0.01).(2) When compared with the ALI group,the expression of PMN-CD18,MDA content,and W/D ratio were all lower in TanshinoneⅡA treatment group(P<0.05) with ameliorated coagulation abnormality(P<0.01).Histopathological morphometry in the lung tissue showed a decrease in the PMN sequestration and the width of alveolar septa(both P<0.01),and an increase in the VV and SV(P<0.05,P<0.01).Conclusion:TanⅡA plays a protective role in LPS-induced lung injury in rats through improving hypercoagulating state,decreasing PMN-CD18 expression and alleviating migration,reducing lipid peroxidation and alleviating pathological changes.     

喘消雾化液对博莱霉素诱导大鼠肺纤维化模型SOD和MDA水平的影响

目的:观察喘消雾化液(CXW)对博莱霉素(BLM)诱导大鼠肺纤维化模型的影响,为肺纤维化的防治提供实验依据。方法:90只雄性Wistar大鼠随机分为生理盐水(NS)组、模型组(BLM组)、CXW组。BLM、CXW组经腹腔注入15mg/kgBLM×10d制作肺纤维化动物模型,分别于第1、14、28天每组各处死10只,留取血液,收集支气管肺泡灌洗液(BALF)进行细胞学计数及其分类;评价各组各时间点肺组织病理形态学变化,定量肺泡间隔宽度;检测肺组织匀浆中羟脯氨酸(HYP)含量;检测血清和肺组织匀浆中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量。结果:(1)与NS组比较,BLM组在第1、14、28天时的肺泡壁厚度、胸膜厚度和肺系数差异均有统计学意义(P均<0.05),CXW组肺泡壁厚度、胸膜厚度明显增加,与BLM组比较差异有统计学意义(P均<0.05)。(2)与同期NS组比较,BLM组第14、28天的HYP含量,第1、14天的细胞总数及炎性细胞比例和肺组织匀浆中MDA含量均明显升高(P均<0.05),第1天肺组织匀浆中SOD活力明显降低(P<0.05)。同期CXW组改变不明显,与BLM组比较,差异均有统计学意义(P均<0.05)。结论:CXW可能通过提高大鼠肺纤维化模型中SOD活力,降低MDA含量,并在一定程度上阻止或延缓了胶原的沉积,起到了保护肺组织的作用。     

Visco-supplementation therapy in internal derangement of temporomandibular joint

OBJECTIVE: To study if visco-supplementation therapy is useful to the internal derangement (ID) of temporomandibular joint (TMJ). METHODS: Sixty-three ID cases (69 TMJs) were studied by visco-supplementation therapy. The upper and/or lower articular cavities were irrigated with 5 ml normal saline and injected 0.3-1.0 ml 1% hyaluronate (HA) into articular cavity. If the symptoms of the disease still existed one week later, the therapy should be repeated for 1-2 times, once a week. The control group cases were injected 1 ml 2% lidocaine instead of HA. 8 other TMJs of 6 ID cases and 2 normal cadavers were studied with scanning electron microscopy (SEM) and light microscopy (LM). RESULTS: The visco-supplement therapy was useful to ID patients. The difference between the test group and control group had statistical significance (chi 2 = 6.6535, P < 0.01). SEM and LM showed that the condyle, disc and bilaminar region in ID were degenerated or destroyed. CONCLUSIONS: The friction between the articular surfaces in ID was increased and the bilaminar region could not retract the disc as in healthy TMJ. The visco-supplementation therapy can decrease the friction and resume the normal rheology of the diseased TMJs.     

补肺阳方对慢性阻塞性肺疾病肺阳虚证模型大鼠的影响

目的研究补肺阳方对慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)肺阳虚证大鼠肺功能的影响,为补肺阳方治疗COPD提供实验研究依据。方法采用烟熏加气管滴注脂多糖及二次造模的方法建立大鼠COPD肺阳虚证模型。将补肺阳方高中低剂量(12.6 g/kg、6.3 g/kg、3.15 g/kg)给予不同组别COPD肺阳虚证大鼠,同时设立正常组及胸腺肽(阳性药物)对照组。利用肺功能仪器检测大鼠肺功能,HE染色法观察气管及肺组织病理学变化,扫描电子显微镜观察气管超微结构变化。结果HE染色显示模型对照组大鼠气管黏膜上皮脱落严重,黏膜下腺体增生,气管壁各层均有大量炎细胞浸润,肺泡隔变薄、断裂,肺泡相互融合形成肺大泡;胸腺肽对照组支气管形态完整,炎性细胞渗出较少;补肺阳方高中低剂量组与模型对照组相比,上皮细胞脱落减轻,炎性渗出物减少。扫描电子显微镜显示模型对照组黏膜不完整,中间有凹陷,形成沟壑状,纤毛非常稀疏,可见明显脱落;补肺阳方不同剂量及胸腺肽对照组病变均较轻。肺功能结果显示,与正常组比较,模型对照组最大通气量(maximum ventilatory volume,MVV)明显降低(P<0.01),第二秒用力呼出容积占用力肺活量百分比(percentage of 0.2 second forced expiratory volume in forced vital capacity,FEV0.2/FVC)下降(P<0.01);与模型对照组比较,补肺阳方各剂量组MVV出现明显上升(P<0.05,P<0.01),但FEV0.2/FVC的变化差异无统计学意义(P>0.05)。结论补肺阳方可显著改善COPD肺阳虚证大鼠的症状和肺功能。     

槲皮素对博莱霉素致鼠肺纤维化的防治作用

目的：观察SD大白鼠腹腔内注射槲皮素对实验性博莱霉素致肺纤维化的防治作用。方法：通过博莱霉素致鼠肺纤维化的动物模型。动态观察各实验组与肺纤维化形成相关的第3、7、14、28天肺组织匀浆羟脯氨酸、脂质过氧化物（LPO）含量,动态观察肺组织病理学变化及形态学定量测量肺组织中炎症细胞数/每高倍视野、肺泡间隔宽度、单位过氧化物（LPO）含量,动态观察肺组织病理学变化及形态学定量测量肺组织中炎症细胞数/每高倍视野、肺泡间隔宽度、单位面积肺纤维化灶所占的分面积。结果：实验组与对照组相比,槲皮素组能显著地降低博莱霉素致肺纤维化程度。结论：槲皮素对博莱霉素致肺纤维化有一定的防治作用。     

Synergistic Anti-inflammatory Effect of Radix Platycodon in Combination with Herbs for Cleaning-heat and Detoxification and Its Mechanism

Objective:To investigate the synergistic anti-inflammatory effect of Radix Platycodon in combination with herbs for cleaning-heat and detoxification and its mechanism for Fei(肺)-targeting.Methods: Forty Wistar rats were randomly divided into five groups(8 per group):the sham-operated group,model group, Radix Platycodon group,Flos Lonicera and Fructus Forsythia(LF) group,and Radix Platycodon,Flos Lonicera and Fructus Forsythia combination(PLF) group,using a random number table.A rat chronic obstructive pulmonary disease(COPD) model was established by passive smoking and intratracheal instillation of lipopolysaccharide(LPS).The treatments started from the 15th day of passive smoking for a total duration of 14 days.At the end of the treatment,changes in the following measurements were determined:lung histopathology, inflammatory cytokines including tumor necrosis factorα(TNF-α),transforming growth factorβ(TGF-β) and interleukin IL-1β(IL-1β) in bronchoalveolar lavage fluid(BALF),and mRNA expression of endogenous active substance intestinal trefoil factor 3(TFF3) in the lung tissue.Results:Light microscopy showed that compared with the sham-operated group,rats in the COPD model group had disrupted alveolar structure,collapsed local alveoli,significantly widened or even fused alveolar septa,and massive infiltration of inflammatory cells in the alveolar wall and interstitium.In addition,significant bronchial epithelium hyperplasia,partially shed epithelia, and marked inflammatory cell infiltration in the bronchial wall and its surrounding tissues were noticed.Electron microscopy showed that rats in the model group had degeneration of alveolar type II epithelial cell;reduction, breakage or even loss of cell surface microvilli;swollen mitochondria with disappearing cristae and vacuole-like structure;and,increased secondary lysosomes in alveolar macrophages.The TNF-α,TGF-βand IL-1βlevels and white blood cell(WBC) count in BALF were significantly increased(P<0.01 or P<0.05) and TFF3 mRNA expression in the lung tissue was significantly reduced(P<0.01).After treatment,the pathological morphology of lung injury was less severe in all three treatment groups.In addition,TGF-βand IL-1βand WBC count in BALF were decreased(P<0.01 or P<0.05),and TFF3 mRNA expression in the lung tissue was significantly increased in the PLF group(P<0.01).Compared with the LF group,the IL-1 p in BALF was significantly decreased (P<0.05),and TFF3 mRNA expression was significantly increased(P<0.05) in the PLF group.Conclusions:Radix Platycodon synergizes with herbs for cleaning-heat and detoxification in reducing inflammatory injury in a rat model of COPD.The synergistic anti-inflammatory effect is reflected in the improvement in pathological changes and in the reduction of IL-1 p levels in BALF.The mechanism of such synergistic action may be related to its effect on maintaining the TFF3 mRNA expression and Fei-targeting function.     

肺通口服液对大鼠肺纤维化模型的治疗作用

①目的　观察肺通口服液对大鼠肺纤维化的治疗作用。②方法　观察不同浓度肺通口服液治疗后大鼠肺纤维化模型肺组织的超氧化物歧化酶 (SOD)的活性、羟脯氨酸 (HP)含量、丙二醛 (MDA)含量及其超微结构的变化等 ,并与对照组进行比较。③结果　大剂量组 (15 g/kg体质量 )第 14、2 8天时的SOD活性、HP含量、MDA含量、炎性细胞的个数、肺泡隔平均宽度及肺通气量 (CO2 、O2 )等指标与模型组比较 ,差异均有显著性 (F =3.0 3～188.0 8,q =3.34～ 37.0 0 ,P <0 .0 5、0 .0 1、0 .0 0 1)。肺通口服液组肺组织的超微结构也较对照组有明显改善。④结论　肺通口服液对大鼠肺纤维化模型具有治疗作用。