The effect of positive end-expiratory pressure on functional residual capacity: role of prostaglandin production.
It has been shown that lung distension can generate prostaglandins. To test the hypothesis that there may be a prostaglandin-mediated peripheral (alveolar duct) bronchodilator effect contributing to the increase in functional residual capacity (FRC) observed with positive end-expiratory pressure (PEEP), we applied PEEP to 8 beagle dogs at 2, 5, 5, 7.5, and 10 cm H2O, and measured FRC at each level and immediately after cessation of PEEP. This experiment was then repeated after the intravenous administration of indomethacin 10 mg/kg. The results indicate a significant reduction of FRC (p less than 0.05) at 5, 7.5, and 10 cm PEEP after the administration of indomethacin. Furthermore, FRC initially failed to return to baseline immediately after cessation of PEEP but did so after indomethacin. We conclude that endogenous prostaglandin production of PEEP but did so after indomethacin. We conclude that endogenous prostaglandin production may be partially responsible for the elevation of FRC with PEEP.[1]References
- The effect of positive end-expiratory pressure on functional residual capacity: role of prostaglandin production. Berend, N., Christopher, K.L., Voelkel, N.F. Am. Rev. Respir. Dis. (1982) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
