Advertisement
Regular Article| Volume 67, ISSUE 2, P193-198, February 01, 1997

Download started.

Ok

Decreased Pulmonary Compliance Is an Early Indicator of Pulmonary Oxygen Injury

DOI:https://doi.org/10.1006/jsre.1996.4980
Decreased Pulmonary Compliance Is an Early Indicator of Pulmonary Oxygen Injury
Previous ArticleTime-Dependent Changes of Serum Gastrin and Gastrin Receptors in the Rat Oxyntic Mucosa after Proximal Gastric Vagotomy
Next ArticleDifferential Effects of IL-1β and Ibuprofen after Endotoxic Challenge in Mice
      This paper is only available as a PDF. To read, Please Download here.

      Abstract

      Pulmonary oxygen injury is classified by the development of tissue and alveolar edema, surfactant dysfunction, lung inflammation, and decreased pulmonary compliance. In neonates prolonged oxygen therapy is associated with the development of bronchopulmonary dysplasia. Recombinant DNA technology makes it possible to experimentally explore the role of specific proteins in the development of pulmonary oxygen injury. However,in vivoexperiments require sensitive ways of identifying pulmonary oxygen injury early in its development. We therefore compared the sensitivities of several experimental assays used to assess pulmonary injury. We found that changes in pulmonary compliance were the most sensitive and showed significant differences after 72 hr of exposure to normobaric hyperoxia (FiO2= 0.95), which correlated with a small change in the histology of the mice lungs. The concentration of protein in the bronchoalveolar lavage fluid was less sensitive and did not differ significantly until after 96 hr of exposure. The survival in hyperoxia also did not worsen until after 96 hr. The lung wet/dry weight ratios was the least sensitive assay and did not increase until after 5 days of exposure to normobaric hyperoxia. We conclude that a decrease in pulmonary compliance is an early indicator of pulmonary oxygen injury and may be a better way to study the mechanisms and mediators of pulmonary oxygen injury.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Journal of Surgical Research
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Register: Create an account
      Institutional Access: Sign in to ScienceDirect

      References

      REFERENCES

        • Wispé J.R.
        • Roberts R.J.
        Molecular basis of pulmonary oxygen toxicity.
        Clinics Pediatr. 1987; 14: 651-666
        • Warner B.B.
        • Wispé J.R.
        Free radical-mediated diseases in pediatrics.
        Semin. Perinatol. 1992; 16: 47-57
        • Jenkinson S.
        Oxygen toxicity.
        New Horizons. 1993; 1: 504-511
        • Nogee L.M.
        • Wispé J.R.
        Effects of pulmonary oxygen injury on airway content of surfactant-associated protein A.
        Pediatr. Res. 1988; 24: 568-573
        • Lindsey H.
        • Kisala J.
        • Ayala A.
        • Lehman D.
        • Herdon C.D.
        • Chaudry I.H.
        Pentoxifylline attenuates oxygen-induced lung injury.
        J. Surg. Res. 1994; 56: 543-548
        • Frank L.
        • Summerville J.
        • Massaro D.
        Protection from oxygen toxicity with endotoxin.
        J. Clin. Invest. 1980; 65: 1104-1110
        • Vacchiano C.
        • Tempel G.
        Role of nonenzymatically generated prostanoid, 8-iso-PGF2 alpha, in pulmonary oxygen toxicity.
        J. Appl. Physiol. 1994; 77: 2912-2917
        • Wispé J.
        • Warner B.
        • Clark J.C.
        • Dey C.R.
        • Neuman J.
        • Glasser S.W.
        • Crapo J.D.
        • Chang C.Y.
        • Whitsett J.A.
        Human Mn-superoxide dismutase in pulmonary epithelial cells of transgenic mice confers protection from oxygen injury.
        J. Biol. Chem. 1992; 267: 23937-23941
        • Majzoub J.
        • Muglia L.
        Knockout mice.
        N. Engl. J. Med. 1996; 334: 904-907
        • Crapo J.D.
        Morphologic changes in pulmonary oxygen toxicity.
        Annu. Rev. Physiol. 1986; 48: 721-731
        • Frank L.
        • Massaro H.
        Oxygen toxicity.
        Am. J. Med. 1980; 69: 117-126
        • Robbins C.G.
        • Davis J.M.
        • Merritt T.A.
        • Amirkhanian J.D.
        • Sahgal N.
        • Morin F.C.
        • Horowitz S.
        Combined effects of nitric oxide and hyperoxia on surfactant function and pulmonary inflammation.
        Am. J. Physiol. 1995; 269: L545-L550
        • Nogee L.M.
        • Wispé J.R.
        • Clark J.C.
        • Weaver T.E.
        • Whitsett J.A.
        Increased expression of pulmonary surfactant proteins in oxygen-exposed rats.
        Am. J. Respir. Cell. Mol. Biol. 1991; 4: 102-107
        • Balaan M.R.
        • Bowman L.
        • Dedhia H.V.
        • Miles P.R.
        Hyperoxia-induced alterations of rat alveolar lavage composition properties.
        Exp. Lung Res. 1995; 21: 141-156
        • Minoo P.
        • Segura L.
        • Coalson J.J.
        • King R.J.
        • DeLemos R.A.
        Alterations in surfactant protein gene expression associated with premature birth and exposure to hyperoxia.
        Am. J. Physiol. 1991; 261: L386-L392
        • Minoo P.
        • King R.J.
        • Coalson J.J.
        Surfactants proteins and lipids are regulated independently during hyperoxia.
        Am. J. Physiol. 1992; 263: L291-L298
        • Holm B.A.
        • Notter R.H.
        • Siegle J.
        • Matalon S.
        Pulmonary physiological and surfactant changes during injury and recovery from hyperoxia.
        J. Appl. Physiol. 1985; 59: 1402-1409
        • Arkovitz M.S.
        • Wispé J.R.
        • Garcia V.F.
        • Szabó C.
        Selective inhibition of the inducible isoform of nitric oxide synthase prevents pulmonary trans-vascular flux during acute endotoxemia.
        J. Pediatr. Surg. 1996; 31: 1009-1015
        • MacMicking J.D.
        • Nathan C.
        • Hom G.
        • Chartrain N.
        • Fletcher D.S.
        • Trumbauer M.
        • Stevens K.
        • Qiao-wen X.
        • Sokol K.
        • Hutchinson N.
        • Chen H.
        • Nudgett J.S.
        Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase.
        Cell. 1995; 81: 641-650

      Article info

      Identification

      DOI: https://doi.org/10.1006/jsre.1996.4980

      Copyright

      © 1997 Academic Press. Published by Elsevier Inc. All rights reserved.

      ScienceDirect

      Access this article on ScienceDirect

      The content on this site is intended for healthcare professionals.


      We use cookies to help provide and enhance our service and tailor content. To update your cookie settings, please visit the Cookie Preference Center for this site.
      Copyright © 2023 Elsevier Inc. except certain content provided by third parties.


      RELX