title: Hyperbaric air exposure at 2.5 ATA does not affect respiratory mechanics and lung histology in the rat.
abstract: BACKGROUND
  We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the "ohmic" and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (hyperbarism) lasting 90 min.
  
  
  METHODS
  We used the end-inflation occlusion method on anesthetized rats after about 15 min from previous exposure to hyperbarism. The method allows the measurements of respiratory system elastance and of the ohmic and viscoelastic components of airway resistance, which respectively depend on the Newtonian pressure dissipation due to the ohmic airway resistance to airflow and on the viscoelastic pressure dissipation caused by respiratory system tissue stress relaxation. The expressions of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in the lung's tissues were also investigated, together with the histological characteristics of lung tissue. Data were compared with those obtained in control animals and in previously studied animals exposed to hyperoxic hyperbarism.
  
  
  RESULTS
  Unlike with hyperoxic hyperbarism, hyperbarism per se did not change significantly the parameters of respiratory mechanics in the control animals (respiratory system elastance and ohmic and viscoelastic resistances were 2.01 ± 0.17 vs. 1.74 ± 0.08 cm H(2)O/ml, and 0.13 ± 0.02 vs. 0.13 ± 0.03 and 0.425 ± 0.04 vs. 0.33 ± 0.03 cm H(2)O/ml s(-1) in control vs. experimental animals, respectively, none significantly different), nor did it induce evident effects on lung histology. An increment of both iNOS and eNOS expressions was documented instead (0.50 ± 0.05 vs. 0.75 ± 0.07 and 1.04 ± 0.1 and 1.4 ± 0.15, respectively).
  
  
  CONCLUSIONS
  Our results indicate that, at variance with hyperoxic hyperbarism, the acute exposure to only hyperbarism does not affect either the elastic or the resistive respiratory system properties, or lung histology.
authors.affiliation: Department of Biomedical Sciences, Section Physiology, University of Padova, Via Marzolo, 3, 35100, Padua, Italy, alessandro.rubini@unipd.it.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Rubini
authors.forename: Andrea
authors.initials: A
authors.lastname: Porzionato
authors.forename: Gloria
authors.initials: G
authors.lastname: Sarasin
authors.forename: Susi
authors.initials: S
authors.lastname: Zara
authors.forename: Veronica
authors.initials: V
authors.lastname: Macchi
authors.forename: Enrico
authors.initials: E
authors.lastname: Camporesi
authors.forename: Gerardo
authors.initials: G
authors.lastname: Bosco
mesh_terms: D000403:Airway Resistance; D000818:Animals; D004548:Elasticity; D005260:Female; D006931:Hyperbaric Oxygenation / Q000009:adverse effects / Q000379:methods*; D008168:Lung / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D023421:Models, Animal; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011312:Pressure; D017208:Rats, Wistar; D015656:Respiratory Mechanics; D018570:Risk Assessment; D013997:Time Factors; D014783:Viscosity
chemical_list: D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat