- 同
- CLE
WordNet
- an abnormal condition of the lungs marked by decreased respiratory function; associated with smoking or chronic bronchitis or old age (同)pulmonary_emphysema
PrepTutorEJDIC
- 気腫(きしゅ),肺気腫
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- 1. 慢性閉塞性肺疾患（COPD）：定義、臨床症状、診断、および病期分類 chronic obstructive pulmonary disease definition clinical manifestations diagnosis and staging
- 2. 肺の高分解能CT high resolution computed tomography of the lungs
- 3. 先天性肺葉性肺気腫 congenital lobar emphysema
- 4. α-1アンチトリプシン欠乏症の臨床症状、診断、および自然経過 clinical manifestations diagnosis and natural history of alpha 1 antitrypsin deficiency
- 5. 慢性閉塞性肺疾患（COPD）の新規治療法：肺気腫の気管支鏡治療 emerging therapies for copd bronchoscopic treatment of emphysema
English Journal
- A comprehensive analysis of oxidative stress in the ozone-induced lung inflammation mouse model.
- Wiegman CH, Li F, Clarke CJ, Jazrawi E, Kirkham P, Barnes PJ, Adcock IM, Chung KF.Author information *Airways Disease Section, National Heart & Lung Institute, Imperial College London, London SW3 6LY, U.K.AbstractOzone is an oxidizing environmental pollutant that contributes significantly to respiratory health. Exposure to increased levels of ozone has been associated with worsening of symptoms of patients with asthma and COPD (chronic obstructive pulmonary disease). In the present study, we investigated the acute and chronic effects of ozone exposure-induced oxidative stress-related inflammation mechanics in mouse lung. In particular, we investigated the oxidative stress-induced effects on HDAC2 (histone deacetylase 2) modification and activation of the Nrf2 (nuclear factor erythroid-related factor 2) and HIF-1α (hypoxia-inducible factor-1α) signalling pathways. Male C57BL/6 mice were exposed to ozone (3 p.p.m.) for 3 h a day, twice a week for a period of 1, 3 or 6 weeks. Control mice were exposed to normal air. After the last exposure, mice were killed for BAL (bronchoalveolar lavage) fluid and lung tissue collection. BAL total cell counts were elevated at all of the time points studied. This was associated with increased levels of chemokines and cytokines in all ozone-exposed groups, indicating the presence of a persistent inflammatory environment in the lung. Increased inflammation and Lm (mean linear intercept) scores were observed in chronic exposed mice, indicating emphysematous changes were present in lungs of chronic exposed mice. The antioxidative stress response was active (indicated by increased Nrf2 activity and protein) after 1 week of ozone exposure, but this ability was lost after 3 and 6 weeks of ozone exposure. The transcription factor HIF-1α was elevated in 3- and 6-week ozone-exposed mice and this was associated with increased gene expression levels of several HIF-1α target genes including Hdac2 (histone deacetylase 2), Vegf (vascular endothelial growth factor), Keap1 (kelch-like ECH-associated protein 1) and Mif (macrophage migration inhibitory factor). HDAC2 protein was found to be phosphorylated and carbonylated in nuclear and cytoplasm fractions, respectively, and was associated with a decrease in DNA-binding activity and protein expression of HDAC2. Decreased HDAC2 activity, most likely a direct result of protein modification, in combination with the loss of the antioxidative stress response and activation of the HIF-1α pathway, contribute to the inflammatory response and emphysema observed in ozone-exposed mice.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Mar 1;126(6):425-40. doi: 10.1042/CS20130039.
- Ozone is an oxidizing environmental pollutant that contributes significantly to respiratory health. Exposure to increased levels of ozone has been associated with worsening of symptoms of patients with asthma and COPD (chronic obstructive pulmonary disease). In the present study, we investigated the
- PMID 24040961
- Recent advances in pre-clinical mouse models of COPD.
- Vlahos R, Bozinovski S.Author information *Lung Health Research Centre, Department of Pharmacology, University of Melbourne, Parkville, VIC 3010, Australia.AbstractCOPD (chronic obstructive pulmonary disease) is a major incurable global health burden and will become the third largest cause of death in the world by 2020. It is currently believed that an exaggerated inflammatory response to inhaled irritants, in particular cigarette smoke, causes progressive airflow limitation. This inflammation, where macrophages, neutrophils and T-cells are prominent, leads to oxidative stress, emphysema, small airways fibrosis and mucus hypersecretion. The mechanisms and mediators that drive the induction and progression of chronic inflammation, emphysema and altered lung function are poorly understood. Current treatments have limited efficacy in inhibiting chronic inflammation, do not reverse the pathology of disease and fail to modify the factors that initiate and drive the long-term progression of disease. Therefore there is a clear need for new therapies that can prevent the induction and progression of COPD. Animal modelling systems that accurately reflect disease pathophysiology continue to be essential to the development of new therapies. The present review highlights some of the mouse models used to define the cellular, molecular and pathological consequences of cigarette smoke exposure and whether they can be used to predict the efficacy of new therapeutics for COPD.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Feb;126(4):253-65. doi: 10.1042/CS20130182.
- COPD (chronic obstructive pulmonary disease) is a major incurable global health burden and will become the third largest cause of death in the world by 2020. It is currently believed that an exaggerated inflammatory response to inhaled irritants, in particular cigarette smoke, causes progressive air
- PMID 24144354
- The composition of cigarette smoke determines inflammatory cell recruitment to the lung in COPD mouse models.
- John G, Kohse K, Orasche J, Reda A, Schnelle-Kreis J, Zimmermann R, Schmid O, Eickelberg O, Yildirim AÖ.Author information *Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Helmholtz Zentrum München, Member of the German Center for Lung Research, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany.AbstractCOPD (chronic obstructive pulmonary disease) is caused by exposure to toxic gases and particles, most often CS (cigarette smoke), leading to emphysema, chronic bronchitis, mucus production and a subsequent decline in lung function. The disease pathogenesis is related to an abnormal CS-induced inflammatory response of the lungs. Similar to active (mainstream) smoking, second hand (sidestream) smoke exposure severely affects respiratory health. These processes can be studied in vivo in models of CS exposure of mice. We compared the acute inflammatory response of female C57BL/6 mice exposed to two concentrations [250 and 500 mg/m3 TPM (total particulate matter)] of sidestream and mainstream CS for 3 days and interpreted the biological effects based on physico-chemical differences in the gas and particulate phase composition of CS. BAL (bronchoalveolar lavage fluid) was obtained to perform differential cell counts and to measure cytokine release. Lung tissue was used to determine mRNA and protein expression of proinflammatory genes and to assess tissue inflammation. A strong acute inflammatory response characterized by neutrophilic influx, increased cytokine secretion [KC (keratinocyte chemoattractant), TNF-α (tumour necrosis factor α), MIP-2 (macrophage inflammatory protein 2), MIP-1α and MCP-1 (monocyte chemoattractant protein-1)], pro-inflammatory gene expression [KC, MIP-2 and MMP12 (matrix metalloproteinase 12)] and up-regulated GM-CSF (granulocyte macrophage colony-stimulating factor) production was observed in the mainstream model. After sidestream exposure there was a dampened inflammatory reaction consisting only of macrophages and diminished GM-CSF levels, most likely caused by elevated CO concentrations. These results demonstrate that the composition of CS determines the dynamics of inflammatory cell recruitment in COPD mouse models. Different initial inflammatory processes might contribute to COPD pathogenesis in significantly varying ways, thereby determining the outcome of the studies.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Feb;126(3):207-21. doi: 10.1042/CS20130117.
- COPD (chronic obstructive pulmonary disease) is caused by exposure to toxic gases and particles, most often CS (cigarette smoke), leading to emphysema, chronic bronchitis, mucus production and a subsequent decline in lung function. The disease pathogenesis is related to an abnormal CS-induced inflam
- PMID 23875733
Japanese Journal
- 右B^1転位気管支領域に限局した肺気腫の1切除例
- 星野 英久,石川 亜紀,門山 周文
- 気管支学 : 日本気管支研究会雑誌 35(4), 424-429, 2013-07-25
- 背景.異常気管支領域には気管支拡張や気管支炎の合併頻度が高いとされている.症例. 33歳,男性.右気胸の診断にて加療目的に当科転院となった.胸部CTで,右肺尖に肺嚢胞が多発しており,また右B^1転位気管支領域に限局して著明な気腫性変化を認めた.術中に肺尖の肺嚢胞より気漏を確認したが,気腫性変化の著明な右S^1を切除する方針とし,胸腔鏡補助下右S^1区域切除術を施行した.病理組織学的には,肺尖の気腫 …
- NAID 110009635596
- 気腫合併肺線維症の病理 : 喫煙関連肺疾患の観点から (特集 気腫合併肺線維症をどう考えるか)
- 武村 民子
- 日本胸部臨床 71(12), 1195-1202, 2012-12
- NAID 40019512769
- 小葉中心性肺気腫の形態形成 : 弾性線維構築および血管構築変容の肺厚切標本および組織再構成による3次元的観察
- 稲垣 卓也,羽野 寛,森川 利昭
- 東京慈恵会医科大学雑誌 127(4), 129-139, 2012-07-15
- NAID 40019427251
Related Links
- centrilobular emphysema n. Emphysema that primarily affects the lobules around their central bronchioles and that is causally related to bronchiolitis. Also called centri-acinar emphysema.
- Centrilobular pulmonary emphysema is the most common morphological subtype of pulmonary emphysema.EpidemiologyIt may be found in up to one-half of adult smokers at autopsy 1.PathologyThe pathological process of ...
Related Pictures
★リンクテーブル★
| リンク元 | 「肺気腫」「小葉中心性肺気腫」 |
| 関連記事 | 「emphysema」「centrilobular」 |
「肺気腫」
- 英
- emphysema, pulmonary emphysema PE
- 同
- 慢性肺気腫 chronic pulmonary emphysema CPE ← 急性肺気腫は存在しない
- 関
- chronic obstructive pulmonary disease
概念
- 肺気腫による気流障害は支持組織としての肺胞が破壊されているため、末梢気道が呼出時に虚脱することと、気道病変の存在による。
定義
- 終末気管支より末梢の気腔が永久的に拡張した状態で、この気腔の壁は破壊されているが線維化はない (1987年アメリカ胸部疾患学会)
- 肺胞壁の破壊的な変化により末梢気管支梢から末梢の含気区域が異常に拡大していることを特徴とする解剖学的変化 (1962 WHO アメリカ胸部疾患学会)
病因
疫学
- 中・高年喫煙者、40歳以上のヘビースモーカーの男子
病型
症状
- 労作時呼吸困難
- 初期には閉塞性換気障害を認めるが、安静時には症状無し
- 労作時に肺胞の破壊による血管床の減少により、拡散障害による低酸素血症をきたし呼吸困難を呈する。
- 咳嗽・喀痰：慢性気管支炎合併例。肺気腫優位型では、咳嗽・喀痰をあまり訴えないことが多い。
身体所見
- 参考1改変
- 視診：
- 呼吸促迫時に口すぼめ呼吸、補助呼吸筋(胸鎖乳突筋の発達)
- 胸郭：過膨張、ビヤ樽状、フーバー徴候(呼気時に両側季肋部が内方へ牽引)
- 触診：
- 気管短縮：輪状軟骨から胸骨柄上縁までの距離が2横指以下 ← たしか、過膨張により気管支が下方に牽引されるため、だったと思う。
- 打診：
- 胸郭：鼓音
- 聴診
- 肺胞呼吸音の減弱 ← たしか、肺胞の破壊のため、だったと思う
検査
動脈血ガス
- PaO2の低下 ← 初期には見られない
- 1) 換気-血流比の不均一分布
- 2) 気相内拡散障害
- 3) 肺胞拡散障害
- PaCO2の上昇 → 病状の進展により、PaO2低下、PaCO2上昇しII型呼吸不全となる。これは、気腫の拡張によりガス交換に関与しない空間(死腔)が拡張する結果、死腔換気となり低酸素血症や高炭酸ガス血症を呈する。
肺機能
- 換気の不均一分布、DLCOの低下。
参考
- 1.
「小葉中心性肺気腫」
「emphysema」
- n.
- ORIGIN mid 17th cent. (sense 2) : via late Latin from Greek emphusēma, from emphusan ‘puff up.’
- puff upは'息を切らす'
「centrilobular」
- adj.
- (肝臓の)小葉中心性の