Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats

中明(Chung-Ming Chen) 陳; Leng-Fang Wang; 綉珠(Hsiu-Chu Chou) 周; 俊松(Jiunn-Song Jiang) 江; 佳衡(Chia-Heng Lin) 林; 文嘉(Wen-Chia Chuang) 莊

Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats

貢獻的翻譯標題: 機械通氣引發的肺傷害會增加大白鼠肺臟的血管收縮素

陳中明(Chung-Ming Chen), Leng-Fang Wang, 周綉珠(Hsiu-Chu Chou), 江俊松(Jiunn-Song Jiang), 林佳衡(Chia-Heng Lin), 莊文嘉(Wen-Chia Chuang)

研究成果: 雜誌貢獻 › 文章 › 同行評審

摘要

我們假設機械通氣導致的肺傷害與肺臟的血管收縮素有關。成年公Sprague-Dawley老鼠隨機分為二組，接受機械通氣兩小時：(1)高潮氣容積(40mL/kg)、零吐氣末陽壓組；(2)低潮氣容積(8mL/kg)、正吐氣末陽壓組(5cmH2O)。沒有接受機械通氣的老鼠當控制組。高潮氣容積、零吐氣末陽壓組的氣管肺泡灌洗液的蛋白含量及肺傷害指數顯著地比控制組和低潮氣容積、正吐氣末陽壓組高。接受機械通氣兩組的氣管肺泡灌洗液的巨噬細胞發炎蛋白質－2和肺臟血管收縮素顯著地高於控制組。所有研究老鼠的肺臟血管收縮素與氣管肺泡灌洗液的巨噬細胞發炎蛋白質－2數值呈正相關。這些結果表示局部血管緊縮素系統與機械通氣導致肺傷害的病理生理機轉有關，並且建議阻斷血管收縮素可能有治療機械通氣導致肺傷害的潛在功效。

貢獻的翻譯標題	機械通氣引發的肺傷害會增加大白鼠肺臟的血管收縮素
原文	英語
頁（從 - 到）	122-129
頁數	8
期刊	中華民國兒童胸腔醫學會雜誌
卷	5
發行號	3
出版狀態	已發佈 - 2007

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http://www.AiritiLibrary.com/Publication/Index/a0000041-200705-5-3-122-129-a

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title = "Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats",

abstract = "We hypothesized that lung injury and inflammation in ventilation-induced lung injury (VILI) are related to angiotensin (Ang) Ⅱ. Adult male Sprague-Dawley rats were randomized to receive two ventilation strategies for 2 hours: 1) the high-volume zero PEEP group (HVZP) was ventilated with a high tidal volume (40mL/kg) and zero positive end expiratory pressure (PEEP); 2) the low-volume with PEEP group (LVP) was ventilated with a low tidal volume (8mL/kg) and PEEP (5cmH2O). Another group which did not receive ventilation served as the control. Total protein in bronchoalveolar lavage fluid (BALF) was significantly higher in HVZP group than in the control and LVP groups. Rats treated with HVZP ventilation had a significantly higher lung injury score than did the control and LVP groups. BALF macrophage inflammatory protein-2 (MIP-2) and lung Ang Ⅱ were significantly higher in HVZP and LVP groups when compared with the control group. Lung Ang Ⅱ correlated positively with MIP-2 in BALF in all study rats. These results indicate that local angiotensin system is involved in the pathogenesis of VILI and suggest that blockade of Ang Ⅱ might have potential therapeutic implications in alleviating VILI.",

keywords = "血管緊縮素, 氣管肺泡灌洗, 巨噬細胞發炎蛋白－2, angiotensin, bronchoalveolar lavage, macrophage inflammatory protein-2",

author = "陳, {中明(Chung-Ming Chen)} and Leng-Fang Wang and 周, {綉珠(Hsiu-Chu Chou)} and 江, {俊松(Jiunn-Song Jiang)} and 林, {佳衡(Chia-Heng Lin)} and 莊, {文嘉(Wen-Chia Chuang)}",

year = "2007",

language = "English",

volume = "5",

pages = "122--129",

journal = "中華民國兒童胸腔醫學會雜誌",

issn = "2221-1837",

publisher = "中華民國兒童胸腔醫學會",

number = "3",

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T1 - Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats

AU - 陳, 中明(Chung-Ming Chen)

AU - Wang, Leng-Fang

AU - 周, 綉珠(Hsiu-Chu Chou)

AU - 江, 俊松(Jiunn-Song Jiang)

AU - 林, 佳衡(Chia-Heng Lin)

AU - 莊, 文嘉(Wen-Chia Chuang)

PY - 2007

Y1 - 2007

N2 - We hypothesized that lung injury and inflammation in ventilation-induced lung injury (VILI) are related to angiotensin (Ang) Ⅱ. Adult male Sprague-Dawley rats were randomized to receive two ventilation strategies for 2 hours: 1) the high-volume zero PEEP group (HVZP) was ventilated with a high tidal volume (40mL/kg) and zero positive end expiratory pressure (PEEP); 2) the low-volume with PEEP group (LVP) was ventilated with a low tidal volume (8mL/kg) and PEEP (5cmH2O). Another group which did not receive ventilation served as the control. Total protein in bronchoalveolar lavage fluid (BALF) was significantly higher in HVZP group than in the control and LVP groups. Rats treated with HVZP ventilation had a significantly higher lung injury score than did the control and LVP groups. BALF macrophage inflammatory protein-2 (MIP-2) and lung Ang Ⅱ were significantly higher in HVZP and LVP groups when compared with the control group. Lung Ang Ⅱ correlated positively with MIP-2 in BALF in all study rats. These results indicate that local angiotensin system is involved in the pathogenesis of VILI and suggest that blockade of Ang Ⅱ might have potential therapeutic implications in alleviating VILI.

AB - We hypothesized that lung injury and inflammation in ventilation-induced lung injury (VILI) are related to angiotensin (Ang) Ⅱ. Adult male Sprague-Dawley rats were randomized to receive two ventilation strategies for 2 hours: 1) the high-volume zero PEEP group (HVZP) was ventilated with a high tidal volume (40mL/kg) and zero positive end expiratory pressure (PEEP); 2) the low-volume with PEEP group (LVP) was ventilated with a low tidal volume (8mL/kg) and PEEP (5cmH2O). Another group which did not receive ventilation served as the control. Total protein in bronchoalveolar lavage fluid (BALF) was significantly higher in HVZP group than in the control and LVP groups. Rats treated with HVZP ventilation had a significantly higher lung injury score than did the control and LVP groups. BALF macrophage inflammatory protein-2 (MIP-2) and lung Ang Ⅱ were significantly higher in HVZP and LVP groups when compared with the control group. Lung Ang Ⅱ correlated positively with MIP-2 in BALF in all study rats. These results indicate that local angiotensin system is involved in the pathogenesis of VILI and suggest that blockade of Ang Ⅱ might have potential therapeutic implications in alleviating VILI.

KW - 血管緊縮素

KW - 氣管肺泡灌洗

KW - 巨噬細胞發炎蛋白－2

KW - angiotensin

KW - bronchoalveolar lavage

KW - macrophage inflammatory protein-2

M3 - Article

SN - 2221-1837

VL - 5

SP - 122

EP - 129

JO - 中華民國兒童胸腔醫學會雜誌

JF - 中華民國兒童胸腔醫學會雜誌

IS - 3

ER -

Ventilation-induced Lung Injury Increases Lung Angiotensin Ⅱ in Rats

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