The role and localization of nitric oxide synthase in neurogenic inflammation of the rat airways

Jae Jeong Shim, Sang Yeub Lee, Seung Heon Lee, J. K. Suh, J. Y. Cho, C. H. Kim, Kwang Ho In, S. H. Yoo, Kyung Ho Kang

Research output: Contribution to journalArticle

Abstract

Background: There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitric oxide synthase (NOS) activity in the neurogenic inflammation of airways. Method: To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine (L-NNA) on plasma extravasation were evaluated in four groups of Sprague-Dawley rats; sham operation group (sham NANC group), electrical vagal stimulation group (NANC2 group), intravenous pretreatment groups with FK224 (1 mg/kg; FK224 group), and L-NNA (1 mg/kg; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells (iNOS), brain (bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results: The results are that plasma extravasation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment (P < 0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224 (P < 0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea (P < 0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion: These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

Original languageEnglish
Pages (from-to)420-433
Number of pages14
JournalTuberculosis and Respiratory Diseases
Volume43
Issue number3
Publication statusPublished - 1996 Jan 1

Fingerprint

FK 224
Neurogenic Inflammation
Trachea
Nitric Oxide Synthase
Nitric Oxide
Endothelium
Coloring Agents
Neurokinin-1 Receptor Antagonists
Antibodies

Keywords

  • airway
  • neurogenic inflammation
  • nitric oxide synthase

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Infectious Diseases

Cite this

The role and localization of nitric oxide synthase in neurogenic inflammation of the rat airways. / Shim, Jae Jeong; Lee, Sang Yeub; Lee, Seung Heon; Suh, J. K.; Cho, J. Y.; Kim, C. H.; In, Kwang Ho; Yoo, S. H.; Kang, Kyung Ho.

In: Tuberculosis and Respiratory Diseases, Vol. 43, No. 3, 01.01.1996, p. 420-433.

Research output: Contribution to journalArticle

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AU - Lee, Sang Yeub

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AU - Cho, J. Y.

AU - Kim, C. H.

AU - In, Kwang Ho

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N2 - Background: There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitric oxide synthase (NOS) activity in the neurogenic inflammation of airways. Method: To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine (L-NNA) on plasma extravasation were evaluated in four groups of Sprague-Dawley rats; sham operation group (sham NANC group), electrical vagal stimulation group (NANC2 group), intravenous pretreatment groups with FK224 (1 mg/kg; FK224 group), and L-NNA (1 mg/kg; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells (iNOS), brain (bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results: The results are that plasma extravasation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment (P < 0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224 (P < 0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea (P < 0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion: These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

AB - Background: There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitric oxide synthase (NOS) activity in the neurogenic inflammation of airways. Method: To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine (L-NNA) on plasma extravasation were evaluated in four groups of Sprague-Dawley rats; sham operation group (sham NANC group), electrical vagal stimulation group (NANC2 group), intravenous pretreatment groups with FK224 (1 mg/kg; FK224 group), and L-NNA (1 mg/kg; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells (iNOS), brain (bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results: The results are that plasma extravasation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment (P < 0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224 (P < 0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea (P < 0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion: These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

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