Effect of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways

Horng Chyuan Lin, Chun Hua Wang, Chih Teng Yu, Kuo Shiung Huang, Chien Ying Liu, Chih Wei Yang, Han Pin Kuo

研究成果: 雜誌貢獻文章同行評審

2 引文 斯高帕斯(Scopus)

摘要

Objective: To investigate the effects of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways. Design: Prospective, randomized, controlled animal study. Setting: Experimental laboratory. Subjects: Male Sprague-Dawley rats weighing 350-500 g. Interventions: The rats were pretreated with NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg) or saline intravenously 4-6 mins before intratracheal administration of tumor necrosis factor-α, 95% oxygen, or both, when the vasopressor effect of L-NAME had reached a plateau. Measurements and Main Results: Bronchoalveolar lavage fluid was recovered from the airway of rats after exposure to 95% oxygen and tumor necrosis factor-α for 6 hrs under ventilator support. Neutrophils in lavage fluid were isolated and examined for the inducible nitric oxide synthase expression by flow-cytometric assay. Tumor necrosis factor-α and interleukin-1β in lavage fluid were measured by enzyme-linked immunosorbent assay. The percentage of neutrophils in bronchoalveolar fluid was significantly higher in rats exposed to hyperoxia + tumor necrosis factor-α (29.7 ± 12.5%) compared with rats with hyperoxia (16.3 ± 1.2%), tumor necrosis factor-α (4.2 ± 1.1%), or room air (5.0 ± 1.8%) alone (p < .05). Rats exposed to hyperoxia + tumor necrosis factor-α had significantly higher concentrations of inducible nitric oxide synthase of neutrophils (350.1 ± 75.7 mean fluorescence intensity), compared with rats with hyperoxia (64.9 ± 1.6 mean fluorescence intensity), tumor necrosis factor-α (102.6 ± 15.3 mean fluorescence intensity), or room air (111.2 ± 25.8 mean fluorescence intensity) alone (p < .05). Rats exposed to hyperoxia + tumor necrosis factor-α significantly produced higher concentrations of tumor necrosis factor-α and interleukin-1β, compared with rats with tumor necrosis factor-α, hyperoxia, or room air alone. Hyperoxia + tumor necrosis factor-α also significantly increased growth-related oncogene/cytokine-induced neutrophil chemoattractant (GRO/CINC)-1 in bronchoalveolar fluid, compared with those receiving tumor necrosis factor-α alone, hyperoxia alone, or room air alone. L-NAME significantly enhanced the percentage of neutrophil recovery and the production of tumor necrosis factor-α, interleukin-1β, and GRO/CINC-1 in airways compared with the corresponding hyperoxia + tumor necrosis factor-α treatment alone. Conclusions: Endogenous nitric oxide may be an important endogenous inhibitor of hyperoxia + tumor necrosis factor-α-induced leukocyte recruitment and subsequently tumor necrosis factor-α, interleukin-1β, and GRO/CINC-1 release.
原文英語
頁(從 - 到)508-516
頁數9
期刊Critical Care Medicine
31
發行號2
DOIs
出版狀態已發佈 - 二月 1 2003
對外發佈Yes

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

指紋 深入研究「Effect of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways」主題。共同形成了獨特的指紋。

引用此