EFFECTS OF MILD HYPOTHERMIA ON VENTILATOR LUNG INJURY AND RAT ACID-INDUCED ACUTE LUNG INJURY MODEL

轻度低温对呼吸机肺损伤及大鼠酸致急性肺损伤模型的影响

基本信息

项目摘要

Recent studies have clarified that mechanical stretching and pressure overload can induce lung injury and HSP70 in some tissues and cells. However, it remains unclear whether HSP70 is induced in stretch-subjected lungs, such as those under mechanical ventilation. The present study was designed to investigate the effects of high peak airway pressure(PAP) ventilation on HSP70 expression in intact rat lungs. Male Sprague-Dawley rats were randomly allocated to one of three groups : non-ventilated(anesthesia alone) control group(NVC) ; PAP 15 cmH_2O group(P15) ; and PAP 30 cmH_2O group(P30). Following the 30 min of pressure-controlled assisted ventilation, HSP70 expression in the P30 group was significantly upregulated in bronchiolar cells and subepithelial tissues at 12 h and this upregulation continued throughout the observation period. In contrast, there were no significant differences between the NVC and P15 groups, although HSP70 was upregulated in the P15 group at all time points. HSP … More 70 was induced by high PAP ventilation, but its specific role and induction mechanism remain unclear.Next he effects of mild hypothermia were studied on the expression of intercellular adhesion molecule-1(ICAM-1) and the accumulation of neutrophils after acid-induced lung injury in the rat. Oxygenation in acid-instilled rats was significantly impaired as compared to that in non-instilled groups, but induction of mild hypothermia gradually improved oxygenation. Expression of ICAM-1 was enhanced in the acid-instilled normothermic group. By contrast, no overexpression of ICAM-1 and its transcript was detected in the acid-instilled hypothermic group. In addition, accumulation of neutrophils was markedly inhibited after exposure to mild hypothermia irrespective of the instillation of acid. Our data suggest that mild hypothermia can inhibit the adhesion, activation, and accumulation of neutrophils in the acute phase of acid-induced lung injury and suggest an approach that might potentially reduce ongoing damage in patients with ARDS.Finally we studied effects of human urinary trypsin Inhibitor(Urinastatin UTI) on acid-induced lung injury. UTI is known to inhibit production of tumor necrosis factor(TNF)-a, which potently stimulates leukocyte activation. The purpose of this study was to clarify whether UTI improves acid-induced lung injury in rats by inhibiting activated leukocytes via TNF-aproduction. UTI significantly improved the OA-induced histological changes for 4 h after OA administration. The OA-induced reduction of PaO2, the increase of pulmonary vascular permeability, and the levels of MPO activity and TNF-a in lung tissues weresignificantly improved in rats administrated UTI. The effects in the leukocytopenia group were similar to those in the UTI-administered group. Less
最近的研究表明,机械拉伸和压力超负荷可导致肺损伤和某些组织和细胞中的HSP70。然而,目前还不清楚热休克蛋白70是否在拉伸作用下的肺中诱导,例如在机械呼吸下的肺。本研究旨在探讨高峰压(PAP)通气对正常大鼠肺组织HSP70表达的影响。雄性SD大鼠随机分为3组:非机械通气组(NVC)、PAP 15cmH2O组(P15)和PAP30cmH2O组(P30)。在压力控制辅助机械通气30min后,P30组HSP70在12h时在细支气管细胞和上皮下组织中的表达显著上调,并持续到整个观察期。相比之下,NVC组和P15组之间没有显著差异,尽管P15组在所有时间点都有HSP70的上调。热休克蛋白…高压性肺泡灌洗(PAP)诱导大鼠肺组织细胞间黏附分子-1(ICAM-1)表达及中性粒细胞积聚的变化。与非酸灌注组相比,酸灌注组大鼠的氧合能力明显受损,但亚低温的诱导逐渐改善了氧合能力。常温酸灌注组ICAM-1表达增强。而酸低温组未检测到ICAM-1及其转录本的过度表达。此外,中性粒细胞的积累在暴露于亚低温后明显受到抑制,而与酸的滴注无关。我们的数据表明,亚低温可以抑制酸性肺损伤急性期中性粒细胞的黏附、激活和聚集,并提出了一种可能减少ARDS患者持续损害的方法。最后,我们研究了人尿胰蛋白酶抑制剂(Urinastatin UTI)对酸诱导肺损伤的影响。众所周知,UTI可以抑制肿瘤坏死因子-a的产生,而肿瘤坏死因子-a可以有效地刺激白细胞的激活。本研究的目的是阐明UTI是否通过抑制活化的白细胞产生肿瘤坏死因子而改善大鼠酸诱导的肺损伤。给药后4h,UTI可明显改善OA所致的组织学改变。给药组大鼠肺组织中MPO活性、肿瘤坏死因子-α水平、肺血管通透性增加、动脉血氧分压(PaO2)降低,肺组织匀浆中MPO活性明显升高。白细胞减少组的效果与UTI给药组相似。较少

项目成果

期刊论文数量(5)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Effect of Urinastatin, a human tripsin inhibitor, on the oleic acid-induced acute lung injury in rats via the inhibition of activated leukocytes
人胰蛋白酶抑制剂乌司他丁通过抑制活化白细胞对油酸诱导的大鼠急性肺损伤的影响
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Koji Ito;Shinichiro Kira;Masakazu Mori;Takayuki Noguchi et al.
  • 通讯作者:
    Takayuki Noguchi et al.
Effect of Urinastatin, a human tripsin inhibitor on the oleic acid -induced acute lung injury in rats via the inhibition of activated leukocytes
人胰蛋白酶抑制剂乌司他丁通过抑制活化白细胞对油酸诱导的大鼠急性肺损伤的影响
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Koji Ito;Shinichiro Kira;Masakazu Mori;Takayuki Noguchi et al.
  • 通讯作者:
    Takayuki Noguchi et al.
Mild hypothermia reduces expression of intercellular adhesion molecule-1 (ICAM-1) and accumulation of neutrophils in rat acid-induced lung injury model.
在大鼠酸诱导的肺损伤模型中,亚低温可降低细胞间粘附分子-1 (ICAM-1) 的表达和中性粒细胞的积累。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Shinichiro Kira;Masakazu Mori;Takayuki Noguchi et al.
  • 通讯作者:
    Takayuki Noguchi et al.
Mild hypothermia reduces expression of intercellular adhesion molecule-1 (ICAM-1) and accumulation of neutrophils in rat acid-induced lung injury model
亚低温降低大鼠酸诱导肺损伤模型中细胞间粘附分子-1(ICAM-1)的表达和中性粒细胞的积累
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Shinichiro Kira;Masakazu Mori;Takayuki Noguchi et al.
  • 通讯作者:
    Takayuki Noguchi et al.
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NOGUCHI Takayuki其他文献

NOGUCHI Takayuki的其他文献

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{{ truncateString('NOGUCHI Takayuki', 18)}}的其他基金

Effects of Newly synthetized antioxydant DHLHZn on Bleomycine induced pulmonary fibrosis
新合成抗氧化剂DHLHZn对博莱霉素诱导肺纤维化的影响
  • 批准号:
    23592673
  • 财政年份:
    2011
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Activation of sensory neurons reduces ischemia/ reperfusion-induced acute renal injury in rats
感觉神经元的激活可减轻大鼠缺血/再灌注引起的急性肾损伤
  • 批准号:
    19592092
  • 财政年份:
    2007
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Effect of abnormal body temperature on ventilator induced lung injury and acute phase reaction
体温异常对呼吸机所致肺损伤及急性时相反应的影响
  • 批准号:
    18591710
  • 财政年份:
    2006
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
MILD HYPOTHERMIA ATTENUATES RAT ACID-INDUCED ACUTE LUNG INJURY MODEL
轻度低温减轻大鼠酸诱导的急性肺损伤模型
  • 批准号:
    12671481
  • 财政年份:
    2000
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
EFFECTS OF INTESTINAL LAVAGE ON PATIENTS WITH SEPTIC MULTIPLE ORGAN FAILURE
肠灌洗对脓毒性多器官衰竭患者的影响
  • 批准号:
    10671425
  • 财政年份:
    1998
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

相似海外基金

Genetics, Epigenetics, and Post-translational Modifications and the Development of Ventilator Induced Lung Injury (VILI)
遗传学、表观遗传学和翻译后修饰以及呼吸机所致肺损伤 (VILI) 的发生
  • 批准号:
    10455906
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Novel Therapeutic Antibody Targeting of Extracellular NAMPT in Ventilator-Induced Lung Injury (VILI)
呼吸机引起的肺损伤 (VILI) 中细胞外 NAMPT 的新型治疗抗体
  • 批准号:
    10026453
  • 财政年份:
    2019
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    $ 2.18万
  • 项目类别:
Novel Therapeutic Antibody Targeting of Extracellular NAMPT in Ventilator-Induced Lung Injury (VILI)
呼吸机引起的肺损伤 (VILI) 中细胞外 NAMPT 的新型治疗抗体
  • 批准号:
    10163254
  • 财政年份:
    2019
  • 资助金额:
    $ 2.18万
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Genetics, Epigenetics, and Post-translational Modifications and the Development of Ventilator-Induced Lung Injury (VILI)
遗传学、表观遗传学和翻译后修饰以及呼吸机所致肺损伤 (VILI) 的发生
  • 批准号:
    10094222
  • 财政年份:
    2018
  • 资助金额:
    $ 2.18万
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Dysregulation of the NFkB/Sox18 Axis During Ventilator-Induced Lung Injury (VILI)
呼吸机引起的肺损伤 (VILI) 期间 NFkB/Sox18 轴失调
  • 批准号:
    10094246
  • 财政年份:
    2018
  • 资助金额:
    $ 2.18万
  • 项目类别:
Differential Roles of Sphingosine 1-Phosphate Receptor PTMs and SNPs in Regulation of Ventilator-Induced Lung Injury (VILI)
1-磷酸鞘氨醇受体 PTM 和 SNP 在调节呼吸机所致肺损伤 (VILI) 中的不同作用
  • 批准号:
    10094250
  • 财政年份:
    2018
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    $ 2.18万
  • 项目类别:
Critical Role of NAMPT and Toll-Like Receptor 4 in Inflammation and Mechanical Ventilator-Induced Lung Injury (VILI)
NAMPT 和 Toll 样受体 4 在炎症和机械呼吸机引起的肺损伤 (VILI) 中的关键作用
  • 批准号:
    10094248
  • 财政年份:
    2018
  • 资助金额:
    $ 2.18万
  • 项目类别:
WISP1 and TLR4 Signaling in ventilator-induced lung injury (VILI)
呼吸机引起的肺损伤 (VILI) 中的 WISP1 和 TLR4 信号转导
  • 批准号:
    8757083
  • 财政年份:
    2014
  • 资助金额:
    $ 2.18万
  • 项目类别:
WISP1 and TLR4 Signaling in ventilator-induced lung injury (VILI)
呼吸机引起的肺损伤 (VILI) 中的 WISP1 和 TLR4 信号转导
  • 批准号:
    8899610
  • 财政年份:
    2014
  • 资助金额:
    $ 2.18万
  • 项目类别:
Title: Molecular Mechanisms of Lung Protection from Ventilator Induced Lung Injury (VILI)
标题:肺保护免受呼吸机引起的肺损伤 (VILI) 的分子机制
  • 批准号:
    200979
  • 财政年份:
    2010
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Operating Grants
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