The role of iNOS inhibitors on lung injury induced by gastrointestinal decontamination agents aspiration

J Mol Histol. 2012 Jun;43(3):351-60. doi: 10.1007/s10735-012-9397-z. Epub 2012 Feb 29.

Abstract

Aspiration is a devastating complication during decontamination procedure in poisoning patients. We have investigated whether S-methylisothiourea protects different pulmonary aspiration gastrointestinal decontamination agent-induced lung injury in rats. Forty-two male Sprague-Dawley rats were assigned to one of six groups (n = 7): normal saline, activated charcoal, polyethylene glycol, normal saline + S-methylisothiourea treated activated charcoal + S-methylisothiourea treated and polyethylene glycol + S-methylisothiourea treated. Normal saline, activated aharcoal and polyethylene glycol were instilled into the lungs. The rats received S-methylisothiourea i.p twice daily for 7 days. Serum surfactant protein D, oxidative stress products and inducible nitric oxide synthase expression in the lung were investigated. The aspiration of activated charcoal significantly increased all histopathological scores (P < 0.01). Only peribronchial inflammatory cell infiltration, alveolar edema, and alveolar histiocytes were increased in the polyethylene glycol groups as compared to the normal saline group (P < 0.05). Pulmonary aspiration increased serum malondialdehyde (P < 0.001), and surfactant protein D (P < 0.05) levels and decreased serum superoxide dismutase levels (P < 0.05). S-methylisothiourea treatment decreased all histopathological scores in the activated charcoal treated S-methylisothiourea group (P < 0.01) and only decreased alveolar edema and alveolar histiocytes in the polyethylene glycol-treated S-methylisothiourea group (P < 0.05). S-methylisothiourea treatment reduced elevated oxidative factors, inducible nitric oxide synthase activity and serum surfactant protein D levels. Our findings showed that S-methylisothiourea may be a protective drug against Activated Charcoal and Polyethylene Glycol-induced lung injury.

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / drug therapy*
  • Acute Lung Injury / enzymology
  • Acute Lung Injury / pathology
  • Administration, Inhalation
  • Animals
  • Charcoal / administration & dosage
  • Charcoal / adverse effects
  • Enzyme Inhibitors / therapeutic use*
  • Gastrointestinal Agents / administration & dosage
  • Gastrointestinal Agents / adverse effects
  • Histiocytes / drug effects*
  • Histiocytes / enzymology
  • Histiocytes / pathology
  • Isothiuronium / analogs & derivatives*
  • Isothiuronium / therapeutic use
  • Lung / drug effects*
  • Lung / enzymology
  • Lung / pathology
  • Male
  • Malondialdehyde / blood
  • Nitric Oxide / biosynthesis
  • Nitric Oxide Synthase Type II / antagonists & inhibitors*
  • Nitric Oxide Synthase Type II / metabolism
  • Oxidative Stress
  • Polyethylene Glycols / administration & dosage
  • Polyethylene Glycols / adverse effects
  • Pulmonary Surfactant-Associated Protein D / blood
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Superoxide Dismutase / blood

Substances

  • Enzyme Inhibitors
  • Gastrointestinal Agents
  • Pulmonary Surfactant-Associated Protein D
  • Reactive Oxygen Species
  • Charcoal
  • Isothiuronium
  • Nitric Oxide
  • Polyethylene Glycols
  • Malondialdehyde
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat
  • Superoxide Dismutase
  • S-methylisothiopseudouronium