Hyperbaric oxygen attenuation of lipopolysaccharide-induced acute lung injury involves heme oxygenase-1

T. Y. Huang, P. S. Tsai, T. Y. Wang, C. L. Huang, Chun Jen Huang

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Background: Hyperbaric oxygen (HBO) attenuates lipopolysaccharide (LPS)-induced acute lung injury. This beneficial effect of HBO involves inhibition of inducible nitric oxide synthase (iNOS) expression and subsequent nitric oxide (NO) biosynthesis. We sought to investigate the role of heme oxygenase-1 (HO-1) on this HBO inhibition of iNOS induction and acute lung injury in septic rat lungs. Methods: Before the experiment, 72 rats were randomly allocated to receive HBO or air treatment. With or without HBO pre-treatment, the rats were further divided into the following subgroups (n = 6): (i) LPS injection, (ii) normal saline (N/S) injection, (iii) hemin (a HO-1 inducer) plus LPS, (iv) hemin alone, (v) tin protoporphyrin (SnPP; a HO-1 inhibitor) plus LPS, and (vi) SnPP alone. All rats were maintained for 6 h and then sacrificed with a high-dose pentobarbital injection. Lung injuries and relevant enzymes expression were thus assayed. Results: Histological analysis, PMNs/alveoli ratio, and wet/dry weight ratio measurements demonstrated that LPS caused significant lung injury and HBO and/or hemin significantly attenuated this LPS-induced lung injury. Increased pulmonary iNOS expression and NO production were associated with lung injury. Induction of HO-1, by HBO and/or hemin, significantly attenuated this LPS-induced iNOS expression and acute lung injury. SnPP, on the contrary, offset the effects of HBO and worsened the LPS-induced lung injury. Conclusions: HBO may act through inhibiting pulmonary iNOS expression to attenuate LPS-induced acute lung injury in septic rats. Furthermore, this HBO attenuation of iNOS expression involves HO-1 induction.

Original languageEnglish
Pages (from-to)1293-1301
Number of pages9
JournalActa Anaesthesiologica Scandinavica
Volume49
Issue number9
DOIs
Publication statusPublished - Oct 2005

Fingerprint

Heme Oxygenase-1
Acute Lung Injury
Lipopolysaccharides
Oxygen
Nitric Oxide Synthase Type II
Lung Injury
Hemin
Lung
Injections
Nitric Oxide
Pentobarbital
Air
Weights and Measures

Keywords

  • HBO
  • HO-1
  • Hyperbaric oxygen
  • iNOS
  • Lipopolysaccharide
  • Lung
  • Rat
  • Sepsis

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Hyperbaric oxygen attenuation of lipopolysaccharide-induced acute lung injury involves heme oxygenase-1. / Huang, T. Y.; Tsai, P. S.; Wang, T. Y.; Huang, C. L.; Huang, Chun Jen.

In: Acta Anaesthesiologica Scandinavica, Vol. 49, No. 9, 10.2005, p. 1293-1301.

Research output: Contribution to journalArticle

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abstract = "Background: Hyperbaric oxygen (HBO) attenuates lipopolysaccharide (LPS)-induced acute lung injury. This beneficial effect of HBO involves inhibition of inducible nitric oxide synthase (iNOS) expression and subsequent nitric oxide (NO) biosynthesis. We sought to investigate the role of heme oxygenase-1 (HO-1) on this HBO inhibition of iNOS induction and acute lung injury in septic rat lungs. Methods: Before the experiment, 72 rats were randomly allocated to receive HBO or air treatment. With or without HBO pre-treatment, the rats were further divided into the following subgroups (n = 6): (i) LPS injection, (ii) normal saline (N/S) injection, (iii) hemin (a HO-1 inducer) plus LPS, (iv) hemin alone, (v) tin protoporphyrin (SnPP; a HO-1 inhibitor) plus LPS, and (vi) SnPP alone. All rats were maintained for 6 h and then sacrificed with a high-dose pentobarbital injection. Lung injuries and relevant enzymes expression were thus assayed. Results: Histological analysis, PMNs/alveoli ratio, and wet/dry weight ratio measurements demonstrated that LPS caused significant lung injury and HBO and/or hemin significantly attenuated this LPS-induced lung injury. Increased pulmonary iNOS expression and NO production were associated with lung injury. Induction of HO-1, by HBO and/or hemin, significantly attenuated this LPS-induced iNOS expression and acute lung injury. SnPP, on the contrary, offset the effects of HBO and worsened the LPS-induced lung injury. Conclusions: HBO may act through inhibiting pulmonary iNOS expression to attenuate LPS-induced acute lung injury in septic rats. Furthermore, this HBO attenuation of iNOS expression involves HO-1 induction.",
keywords = "HBO, HO-1, Hyperbaric oxygen, iNOS, Lipopolysaccharide, Lung, Rat, Sepsis",
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KW - Lipopolysaccharide

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KW - Rat

KW - Sepsis

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