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

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)508-516
Number of pages9
JournalCritical Care Medicine
Volume31
Issue number2
DOIs
Publication statusPublished - Feb 1 2003
Externally publishedYes

Fingerprint

Hyperoxia
Nitric Oxide
Tumor Necrosis Factor-alpha
Cytokines
Neutrophils
NG-Nitroarginine Methyl Ester
Interleukin-1
Chemotactic Factors
Fluorescence
Air
Oncogenes
Therapeutic Irrigation
Nitric Oxide Synthase Type II
Growth
Oxygen
Bronchoalveolar Lavage Fluid
Mechanical Ventilators

Keywords

  • Hyperoxia
  • Inducible nitric oxide synthase
  • Interleuken-1β
  • Neutrophils
  • Nitric oxide
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Effect of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways. / Lin, Horng Chyuan; Wang, Chun Hua; Yu, Chih Teng; Huang, Kuo Shiung; Liu, Chien Ying; Yang, Chih Wei; Kuo, Han Pin.

In: Critical Care Medicine, Vol. 31, No. 2, 01.02.2003, p. 508-516.

Research output: Contribution to journalArticle

Lin, Horng Chyuan ; Wang, Chun Hua ; Yu, Chih Teng ; Huang, Kuo Shiung ; Liu, Chien Ying ; Yang, Chih Wei ; Kuo, Han Pin. / Effect of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways. In: Critical Care Medicine. 2003 ; Vol. 31, No. 2. pp. 508-516.
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abstract = "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.",
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T1 - Effect of endogenous nitric oxide on hyperoxia and tumor necrosis factor-α-induced leukosequestration and proinflammatory cytokine release in rat airways

AU - Lin, Horng Chyuan

AU - Wang, Chun Hua

AU - Yu, Chih Teng

AU - Huang, Kuo Shiung

AU - Liu, Chien Ying

AU - Yang, Chih Wei

AU - Kuo, Han Pin

PY - 2003/2/1

Y1 - 2003/2/1

N2 - 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.

AB - 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.

KW - Hyperoxia

KW - Inducible nitric oxide synthase

KW - Interleuken-1β

KW - Neutrophils

KW - Nitric oxide

KW - Tumor necrosis factor-α

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