Increased nitric oxide in exhaled gas as an early marker of lung inflammation in a model of sepsis.
Increased nitric oxide in exhaled gas as an early marker of lung inflammation in a model of sepsis.
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呼出气体中一氧化氮的增加是脓毒症模型中肺部炎症的早期标志。
DOI：
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发表时间：
1995
影响因子：
24.7
通讯作者：
Arthur S Slutsky
中科院分区：
文献类型：
--
作者：
T. Stewart;F. Valenza;S. P. Ribeiro;A. Wener;G. Volgyesi;J. Mullen;Arthur S Slutsky
一氧化氮（NO）与败血症的病理性血管扩张有关。因为NO可以在动物和人类呼出的气体中测量到，我们假设在化粪池模型中呼出的NO会增加。采用盲法设计，将10只雄性Sprague-Dawley大鼠（300 ~ 400 g）麻醉、麻痹、切开气管，随机（5只/组）静脉注射脂多糖（LPS）（伤寒沙门氏菌，20 mg/kg）或安慰剂（等量生理盐水）。随后，收集呼出气体，在通气过程中每隔20 min用化学发光法测定NO浓度（RR 40次/min， VT 3 ml; PEEP 0, FIO2 0.21），持续300 min。另一组10只动物（5只LPS， 5只对照组）以同样的方式处理，然后在240分钟时杀死，并取动脉血样本进行血气和TNF α测定。构建压力体积（PV）曲线，切除、保存肺，并提交组织学评估。lps处理大鼠平均动脉压低于对照组，p < 0.0001。两组肺静态顺应性和PV曲线无明显差异。LPS组TNF α水平（1.40 +/- 0.24 ng/ml）高于对照组（0.09 +/- 0.04 ng/ml）， p < 0.001。与对照组相比，所有lps处理大鼠呼出的NO浓度在约100 min时升高，在约160 min时达到平台，是对照组的6倍（p < 0.0001）。脂多糖组肺间质、空腔及全肺损伤明显加重（p = 0.01）。（摘要删节250字）
Nitric Oxide (NO) has been implicated in the pathologic vasodilation of sepsis. Because NO can be measured in the exhaled gas of animals and humans, we hypothesized that increases in exhaled NO would occur in a septic model. Using a blinded design, 10 male Sprague-Dawley rats (300 to 400 g) were anesthetized, paralyzed, tracheotomized, and randomized (5/group) to receive an intravenous injection of either lipopolysaccharide (LPS) (Salmonella typhosa, 20 mg/kg) or placebo (equal volume of saline). Thereafter, exhaled gas was collected and measurements of NO concentration were made using chemiluminescence every 20 min for 300 min during ventilation (RR 40 breaths/min, VT 3 ml; PEEP 0, FIO2 0.21). Another group of 10 animals (5 LPS; 5 control) were treated in the same fashion and then killed at 240 min and an arterial blood sample obtained for blood gas and TNF alpha determinations. Pressure volume (PV) curves were constructed and lungs removed, preserved, and submitted for histologic evaluation. LPS-treated rats had lower mean arterial pressures than the control group, p < 0.0001. No significant differences in static lung compliance and PV curves were found in the two groups. TNF alpha levels were greater in the LPS group (1.40 +/- 0.24 ng/ml) versus control group (0.09 +/- 0.04 ng/ml), p < 0.001. By contrast to the control group, exhaled NO concentration rose in all LPS-treated rats at approximately 100 min and at about 160 min reached a plateau that was 6 times greater than control levels (p < 0.0001). There was greater interstitial, airspace, and total lung injury in the LPS group (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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肺损伤的机制。
影响因子：
5.7
作者：
Brigham,KL
通讯作者：
Brigham,KL
吸入肺部刺激物后，大鼠肺泡巨噬细胞产生一氧化氮的增加与一氧化氮合酶表达的增加有关。
DOI：
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发表时间：
1993
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Pendino,KJ;Laskin,JD;Shuler,RL;Punjabi,CJ;Laskin,DL
通讯作者：
Laskin,DL
吸入一氧化氮对仔猪 B 族链球菌败血症的影响。
DOI：
10.1164/ajrccm/147.5.1080
发表时间：
1993
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Berger,JI;Gibson,RL;Redding,GJ;Standaert,TA;Clarke,WR;Truog,WE
通讯作者：
Truog,WE
影响因子：
5.4
作者：
Shinbori, T;Walczak, H;Krammer, PH
通讯作者：
Krammer, PH
影响因子：
158.5
作者：
ROSSAINT, R;FALKE, KJ;ZAPOL, WM
通讯作者：
ZAPOL, WM