NDLI: Nitric oxide mediates acute lung injury caused by fat embolism in isolated rat's lungs.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kao, Shang-Jyh Chen, Hsing I.
Description	Country affiliation: Taiwan Author Affiliation: Kao SJ ( Division of Chest Medicine, Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, and School of Respiratory Therapy, Taipei Medical University and Fu-Jen Catholic Medical College, Taipei, Taiwan.)
Abstract	BACKGROUND: The involvement of nitric oxide (NO) in acute lung injury (ALI) induced by fat embolism (FE) has not been investigated. The present study elucidated the role of NO in ALI because of FE. METHODS: FE was produced by introduction of fatty acid (corn oil micelles) into the isolated rat's lungs. Nonselective NO synthase (NOS) and selective inducible NOS (iNOS) inhibitors, N-nitro-l-arginine methyl ester (l-NAME) and l-N(1-iminoethyl)-lysine (l-Nil) as well as NO donors, sodium nitroprusside (SNP), and S-nitroso-N-acetylpenicillamine (SNAP) at a dose of 10 mol/L were given 60 minutes before FE. There were six groups of isolated lungs randomly assigned to receive vehicle (physiologic saline solution), FE, FE with pretreatment of l-NAME, l-Nil, SNP, or SNAP. Each group was observed for 4 hours. RESULTS: FE significantly increased the lung weight changes, pulmonary arterial pressure, and microvascular permeability. The concentration of nitrate or nitrite, methyl guanidine, tumor necrosis factor-alpha, and interleukin-1beta was significantly elevated after FE. Hisotopathologic examination revealed lung edema with multiple fatty droplets in lung tissue. Pretreatment with l-NAME or l-Nil attenuated, whereas SNP or SNAP exacerbated most of the FE-induced changes. Addition of NO donors (SNP or SNAP) into the isolated lungs did not produce significant changes in the lungs, suggesting that NO donation alone without FE does not exerts harmful effect. CONCLUSIONS: Our results suggest that NO production through the iNOS isoform plays a detrimental role in the FE-induced ALI. Free radical and proinflammatory cytokines may also be involved in the pathogenesis of ALI because of FE.
File Format	HTM / HTML
ISSN	00225282
Issue Number	2
Volume Number	64
e-ISSN	15298809
Journal	The Journal of Trauma: Injury, Infection, and Critical Care
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2008-02-01
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Bronchoalveolar Lavage Fluid Research Support, Non-u.s. Gov't Embolism, Fat Body Weight Respiratory Distress Syndrome, Adult Complications Lung Organ Size Rats Rats, Sprague-dawley Male Nitric Oxide Metabolism Discipline Traumatology Journal Article Nitric Oxide Donors Pathology Chemistry Animals Etiology Pulmonary Embolism
Content Type	Text
Resource Type	Article
Subject	Surgery Critical Care and Intensive Care Medicine

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