Cellular changes in bronchoalveolar lavage fluid
in hyperoxia-induced lung injury
HE Xinbiao1, ZHAO Wei2
Author information+
1.Department of Emergency, The Second Hospital, Tianjin Medical University; 2.Institute of Public Health, Tianjin Medical University;
Show less
History+
Published
05 Dec 2008
Issue Date
05 Dec 2008
Abstract
It is well known that high concentration oxygen exposure is a model of acute lung injury (ALI). However, controversy exists over the mechanism. This study was designed to clarify the cellular characteristics in bronchoalveolar lavage fluid (BALF) and body weight loss of rats exposed to oxygen(> 90%). Young male Wistar rats, aged 6 weeks, were divided into three groups: (1) room air group (exposed to room air, n = 22); (2) hyperoxia < 48 h group (exposed to over 90% oxygen for less than 48 h, n = 18); (3) hyperoxia 66–72 h group (exposed to over 90% oxygen for 66–72 h group, n = 7). Compared to the room air group, the total cell counts in the hyperoxia 66–72 h group decreased, whereas the neutrophils increased significantly. The body weights of the rats exposed to room air continued to increase. However, the body weights of oxygen-exposed rats increased slightly on the first day and weight loss was seen from the second day. All rats were noted to have bilateral pleural effusion in the hyperoxia 66–72 h group. The data suggests that (1) an increase in neutrophil count is an evident feature of hyperoxia-induced lung injury; (2) high concentration oxygen exposure can give rise to anorexia and malnutrition, which may play a role in hyperoxia-induced lung injury. Blocking neutrophil influx into lung tissue in the early phase and improving malnutrition are two effective methods to reduce hyperoxic lung injury.
HE Xinbiao, ZHAO Wei.
Cellular changes in bronchoalveolar lavage fluid
in hyperoxia-induced lung injury. Front. Med., 2008, 2(4): 370‒373 https://doi.org/10.1007/s11684-008-0071-5
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
This is a preview of subscription content, contact us for subscripton.
References
1. Valenca S S, Kloss M L, Bezerra F S, Lanzetti M, Silva F L, Porto L C . Effects of hyperoxia on Wistar rat lungs. J Bras Pneumol, 2007, 33(6): 655–662. doi:10.1590/S1806-37132007000600008 2. Desai L P, Sinclair S E, Chapman K E, Hassid A, Waters C M . High tidal volume mechanical ventilationwith hyperoxia alters alveolar type II cell adhesion. Am J Physiol Lung Cell Mol Physiol, 2007, 293(3): 769–778. doi:10.1152/ajplung.00127.2007 3. Pagano A, Metrailler R I, Aurrand L M, Lucattelli M, Donati Y, Argiroffo C B . Poly(ADP-ribose) polymerase-1 (PARP-1) controls lungcell proliferation and repair after hyperoxia-induced lung damage. Am J Physiol Lung Cell Mol Physiol, 2007, 293(3): 619–629. doi:10.1152/ajplung.00037.2007 4. Altemeier W A, Sinclair S E . Hyperoxia in the intensivecare unit: why more is not always better. Curr Opin Crit Care, 2007, 13(1): 73–78. doi:10.1097/MCC.0b013e32801162cb 5. Downey G P, Dong Q, Kruger J, Dedhar S, Cherapanov V . Regulation of neutrophil activation inacute lung injury. Chest, 1999, 116(1 Suppl): 46S–54S 6. Auten R L, Whorton M H, Mason S N . Blocking neutrophil influx reduces DNA damage in hyperoxia-exposednewborn rat lung. Am J Respir Cell MolBoil, 2002, 26(4): 391–397 7. Perkowski S, Scherpereel A, Murciano J C, Arguiri E, Solomides C C, Albelda S M, Muzykantov V, Christofidou S M . Dissociation between alveolartransmigration of neutrophils and lung injury in hyperoxia. Am J Physiol Lung Cell Mol Physiol, 2006, 291(5): 1050–1058. doi:10.1152/ajplung.00067.2006 8. Mackarel A J, Cottell D C, Russell K J, Gerald M X, Connor C M . Migration of neutrophils across humanpulmonary endothelial cells is not blocked by matrix metalloproteinaseor serine protease inhibitors. Am J RespirCell Mol Biol, 1999, 20(6): 1209–1219 9. Lee W L, Downey G P . Leukocyte elastase: physiologicalfunctions and role in acute lung injury. Am J Respir Crit Care Med, 2001, 164(5): 896–904 10. Hirche T O, Atkinson J J, Bahr S, Belaaouaj A . Deficiencyin neutrophil elastase does not impair neutrophil recruitment to inflamedsites. Am J Respir Cell Mol Biol, 2004, 30(4): 576–584. doi:10.1165/rcmb.2003-0253OC 11. Delacourt C, Herigault S, Delclaux C, Poncin A, Levame M, Harf A, Saudubray F, Lafuma C . Protection against acute lung injury by intravenous orintratracheal pretreatment with EPI-HNE-4, a new potent neutrophilelastase inhibitor. Am J Respir Cell MolBiol, 2002, 26(3): 290–297 12. Yamada M, Kubo H, Kobayashi S, Ishizawa K, Sasaki H . Interferon-γ: a keycontributor to hyperoxia-induced lung injury in mice. Am J Physiol Lung Cell Mol Physiol, 2004, 287(5): L1042–L1047. doi:10.1152/ajplung.00155.2004 13. Deng H, Mason S N, Auten R L . Lung inflammation in hyperoxia can be prevented by anti-chemokinetreatment in newborn rats. Am J RespirCrit Care Med, 2000, 162(6): 2316–2323 14. Vozzelli M A, Mason S N, Whorton M H, Auten R L . Antimacrophagechemokine treatment prevents neutrophil and macrophage influx in hyperoxia-exposednewborn rat lung. Am J Physiol Lung CellMol Physiol, 2004, 286(3): L488–493. doi:10.1152/ajplung.00414.2002 15. Peterson M W, Walter M E, Nygaard S D . Effect of neutrophil mediators on epithelial permeability. Am J Respir Cell Mol Biol, 1995, 13(6): 719–727 16. Fischer B M, Voynow J A . Neutrophil elastase inducesMUC5AC gene expression in airway epithelium via a pathway involvingreactive oxygen species. Am J Respir CellMol Biol, 2002, 26(4): 447–452 17. Aoshiba K, Yasuda K, Yasui S, Tamaoki J, Nagai A . Serine proteases increaseoxidative stress in lung cells. Am J PhysiolLung Cell Mol Physiol, 2001, 281(3): L556–564 18. Bhandari V, Choo W R, Homer R J, Elias J A . Increasedhyperoxia-induced mortality and acute lung injury in IL-13 null mice. J Immunol, 2007, 178(8): 4993–5000 19. Bellmeyer A, Martino J M, Chandel N S, Scott G R, Dean D A, Mutlu G M . Leptin resistance protects mice from hyperoxia-induced acute lunginjury. Am J Respir Crit Care Med, 2007, 175(6): 587–594. doi:10.1164/rccm.200603-312OC 20. Barazzone-Argiroffo C, Muzzin P, Donati Y R, Kan C D, Aubert M L, Piguet P F . Hyperoxia increases leptin production: a mechanism mediated throughendogenous elevation of corticosterone. Am J Physiol Lung Cell Mol Physiol, 2001, 281(5): L1150–L1156 21. Factor P, Ridge K, Alverdy J, Jacob I . Continuousenteral nutrition attenuates pulmonary edema in rats exposed to 100%oxygen. J Appl Physiol, 2000, 89(5): 1759–1765 22. Yamaoka S, Kim H S, Ogihara T, Oue S, Takitani K, Yoshida Y, Tamai H . Severe vitamin E deficiencyexacerbates acute hyperoxic lung injury associated with increasedoxidative stress and inflammation. FreeRadic Res, 2007, 42(6): 602–612. doi:10.1080/10715760802189864
AI Summary 中Eng×
Note: Please note that the content below is AI-generated. Frontiers Journals website shall not be held liable for any consequences associated with the use of this content.