The online version of this article (doi:10.1186/1471-2253-14-86) contains supplementary material, which is available to authorized users.
Humberto S Machado, Catarina S Nunes, Paula Sá, Antonio Couceiro, Álvaro Moreira da Silva and Artur Águas contributed equally to this work.
No financial or non-financial competing interests are relevant to any of the authors. Thus, all the authors have no competing interests of any kind regarding the publication of this study.
HM elaborated the study design, experimental laboratory work, the writing of manuscript and editing work. CN performed the statistical advising and calculations, participated in writing of manuscript and editing work. PS participated in the study design, writing and editing of the manuscript. AC participated in the study design and made histological observation of lung preparations. AS participated in the study design, editing and revision of manuscript. AA participated in the study design, laboratory work, editing and revision of manuscript. All authors read and have given final approval of the version to be published; in addition, all authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Mechanical ventilation is a well–known trigger for lung inflammation. Research focuses on tidal volume reduction to prevent ventilator-induced lung injury. Mechanical ventilation is usually applied with higher than physiological oxygen fractions. The purpose of this study was to investigate the after effect of oxygen supplementation during a spontaneous ventilation set up, in order to avoid the inflammatory response linked to mechanical ventilation.
A prospective randomised study using New Zealand rabbits in a university research laboratory was carried out. Rabbits (n = 20) were randomly assigned to 4 groups (n = 5 each group). Groups 1 and 2 were submitted to 0.5 L/min oxygen supplementation, for 20 or 75 minutes, respectively; groups 3 and 4 were left at room air for 20 or 75 minutes. Ketamine/xylazine was administered for induction and maintenance of anaesthesia. Lungs were obtained for histological examination in light microscopy.
All animals survived the complete experiment. Procedure duration did not influence the degree of inflammatory response. The hyperoxic environment was confirmed by blood gas analyses in animals that were subjected to oxygen supplementation, and was accompanied with lower mean respiratory rates. The non-oxygen supplemented group had lower mean oxygen arterial partial pressures and higher mean respiratory rates during the procedure. All animals showed some inflammatory lung response. However, rabbits submitted to oxygen supplementation showed significant more lung inflammation (Odds ratio = 16), characterized by more infiltrates and with higher cell counts; the acute inflammatory response cells was mainly constituted by eosinophils and neutrophils, with a relative proportion of 80 to 20% respectively. This cellular observation in lung tissue did not correlate with a similar increase in peripheral blood analysis.
Oxygen supplementation in spontaneous breathing is associated with an increased inflammatory response when compared to breathing normal room air. This inflammatory response was mainly constituted with polymorphonuclear cells (eosinophils and neutrophils). As confirmed in all animals by peripheral blood analyses, the eosinophilic inflammatory response was a local organ event.
Hemmes SNT, Paulus F, Schultz MJ: From the dark side of ventilation toward a brighter look at lungs. Crit Care Med. 2013, 41: 1296-1304. 10.1097/CCM.0b013e3182771516. CrossRef
Kilpatrick B, Slinger P: Lung protective strategies in anaesthesia. Br J Anaest. 2010, 105: 108-116. 10.1093/bja/aeq299. CrossRef
Guarracino F, Baldassar R: Perioperative acute lung injury: reviewing the role of anesthetic management. J Anesthe Clinical Res. 2012, 4: 312-
De Conno E, Steurer MP, Wittlinger M, Zalunardo MP, Weder W, Schneiter D, Schimmer RC, Klaghofer R, Neff TA, Schmid ER, Spahn DR, Z’graggen BR, Urner M, Beck-Schimmer B: Anesthetic-induced improvement of the inflammatory response to one-lung ventilation. Anesthesiology. 2009, 110: 1316-1326. 10.1097/ALN.0b013e3181a10731. CrossRefPubMed
Britt RD, Velten M, Tipple TE, Nelin LD, Rogers LK: Cyclooxygenase-2 in newborn hyperoxic lung injury. Free Radic Biol Med. 2013, 25: 502-511. CrossRef
Nowak-Machen M, Schmelzle M, Hanidziar D, Junger W, Exley M, Otterbein L, Wu Y, Csizmadia E, Doherty G, Sitkovsky M, Robson SC: Pulmonary NKT cells play an essential role in mediating hyperoxic acute lung injury. Am J Respir Cell Mol Biol. 2013, 48: 601-609. 10.1165/rcmb.2012-0180OC. CrossRefPubMedPubMedCentral
Lamagna C, Scapini P, A. van Ziffle J, DeFranco AL, Lowell CA: Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation. PNAS. 2013, 110: E3311-E3320. 10.1073/pnas.1300617110. Supporting information http://www.pnas.org/lookup/suppl/doi:10.1073/pnas.1300617110/-/DCSupplemental CrossRefPubMedPubMedCentral
Mead R: The Design of Experiments. 1988, Cambridge, New York: Cambridge University Press, 620-1
Suzuki Y, Nishio N, Takeshita K, Takeuchi O, Watanabe K, Sato N, Naoki K, Kudo H, Aoki T, Yamaguchi K: Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2000, 278: L245-L252. PubMed
Quin DA, Moufarrej RK, Volokhov A, Hales CA: Interactions of lung stretch, hyperoxia, and MIP-2 production in ventilator-induced lung injury. J Appl Physiol. 2002, 93: 517-525. CrossRef
Haase VH, Colgan SP, Karhausen J: Inflammatory hypoxia. Cell Cycle. 2005, 4: 256-268. PubMed
Nissim Ben Efraim AH, Eliashar R, Levi-Schaffer F: Hypoxia modulates human eosinophil function. Clin Mol Allergy. 2010, 19; 8: 10- CrossRef
Kopterides P, Kapetanakis T, Siempos II, Magkou C, Pelekanou A, Tsaganos T, Giamarellos-Bourboulis E, Roussos C, Armaganidis A: Short-term administration of a high oxygen concentration is not injurious in an ex-vivo rabbit model of ventilator-induced lung injury. Anesth Analg. 2009, 108: 556-564. 10.1213/ane.0b013e31818f10f7. CrossRefPubMed
- Increased lung inflammation with oxygen supplementation in tracheotomized spontaneously breathing rabbits: an experimental prospective randomized study
Humberto S Machado
Catarina S Nunes
Álvaro Moreira da Silva
- BioMed Central
Neu im Fachgebiet AINS
Meistgelesene Bücher aus dem Fachgebiet AINS
Mail Icon II