The effects of long-term conventional mechanical ventilation on the lungs of adult rats

被引:16
作者
Bailey, Timothy C. [1 ]
Maruscak, Adam A. [1 ]
Martin, Erica L. [1 ]
Forbes, Amy R. [1 ]
Petersen, Anne [1 ]
McCaig, Lynda A. [1 ]
Yao, Li-Juan [1 ]
Lewis, James F. [1 ]
Veldhuizen, Ruud A. W. [1 ]
机构
[1] Univ Western Ontario, Dept Med, Lawson Hlth Res Inst, Dept Physiol & Pharmacol, London, ON, Canada
关键词
biotrauma; mechanical ventilation; pulmonary surfactant;
D O I
10.1097/CCM.0b013e318180b65c
中图分类号
R4 [临床医学];
学科分类号
1002 [临床医学]; 100602 [中西医结合临床];
摘要
Background., Ventilation-induced lung injury is often studied in animal models by using ventilation strategies with high-tidal volumes and high-oxygen concentration over a relatively short period of time. The injury induced by these ventilation strategies includes alterations to the surfactant system and up-regulation of inflammatory markers. Whether these responses to ventilation occur with more clinically relevant ventilation strategies is not known. Objective: To assess how healthy adult rats respond to 24 hrs of conventional mechanical ventilation with respect to lung physiology, markers of inflammation, and alterations to pulmonary surfactant, and how this is affected by the oxygen concentration. Interventions. Adult rats were mechanically ventilated for 24 hrs with a tidal volume of 8 mL/kg, 5 cm H2O positive end-expiratory pressure, at 60 breaths/min with either 21% or 100% oxygen. Animals were monitored for blood oxygenation and other physiologic parameters. After ventilation, lungs were lavaged and analyzed for inflammatory markers and pulmonary surfactant. These outcomes were compared with measurements obtained from spontaneously breathing rats exposed to either 21% or 100% oxygen for 24 hrs. Main Results: Twenty-four hours of ventilation did not result in significant changes in blood oxygenation. Inflammatory markers, such as interleukin-6 concentration and the number of neutrophils in the lavage, were increased in ventilated animals compared with the nonventilated controls, regardless of the level of inspired oxygen. The amount of active surfactant was increased after ventilation; however, the surface activity of this material was impaired as compared with controls. Conclusion: Prolonged mechanical ventilation of health lungs with a physiologically benign strategy can contribute to the inflammatory response and cause alterations to pulmonary surfactant.
引用
收藏
页码:2381 / 2387
页数:7
相关论文
共 38 条
[1]
Decreased pulmonary compliance is an early indicator of pulmonary oxygen injury [J].
Arkovitz, MS ;
Garcia, VF ;
Szabo, C ;
McConnell, K ;
Bove, K ;
Wispe, JR .
JOURNAL OF SURGICAL RESEARCH, 1997, 67 (02) :193-198
[2]
High oxygen concentrations predispose mouse lungs to the deleterious effects of high stretch ventilation [J].
Bailey, TC ;
Martin, EL ;
Zhao, L ;
Veldhuizen, RAW .
JOURNAL OF APPLIED PHYSIOLOGY, 2003, 94 (03) :975-982
[3]
HYPEROXIA-INDUCED ALTERATIONS OF RAT ALVEOLAR-LAVAGE COMPOSITION AND PROPERTIES [J].
BALAAN, MR ;
BOWMAN, L ;
DEDHIA, HV ;
MILES, PR .
EXPERIMENTAL LUNG RESEARCH, 1995, 21 (01) :141-156
[4]
BLIGH EG, 1959, CAN J BIOCHEM PHYS, V37, P911
[5]
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. [J].
Brower, RG ;
Matthay, MA ;
Morris, A ;
Schoenfeld, D ;
Thompson, BT ;
Wheeler, A ;
Wiedemann, HP ;
Arroliga, AC ;
Fisher, CJ ;
Komara, JJ ;
Perez-Trepichio, P ;
Parsons, PE ;
Wolkin, R ;
Welsh, C ;
Fulkerson, WJ ;
MacIntyre, N ;
Mallatratt, L ;
Sebastian, M ;
McConnell, R ;
Wilcox, C ;
Govert, J ;
Thompson, D ;
Clemmer, T ;
Davis, R ;
Orme, J ;
Weaver, L ;
Grissom, C ;
Eskelson, M ;
Young, M ;
Gooder, V ;
McBride, K ;
Lawton, C ;
d'Hulst, J ;
Peerless, JR ;
Smith, C ;
Brownlee, J ;
Pluss, W ;
Kallet, R ;
Luce, JM ;
Gottlieb, J ;
Elmer, M ;
Girod, A ;
Park, P ;
Daniel, B ;
Gropper, M ;
Abraham, E ;
Piedalue, F ;
Glodowski, J ;
Lockrem, J ;
McIntyre, R .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) :1301-1308
[6]
Pulmonary surfactant protein-A (SP-A) restores the surface properties of surfactant after oxidation by a mechanism that requires the Cys6 interchain disulfide bond and the phospholipid binding domain [J].
Capote, KR ;
McCormack, FX ;
Possmayer, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (23) :20461-20474
[7]
Ventilator-induced lung injury - Lessons from experimental studies [J].
Dreyfuss, D ;
Saumon, G .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1998, 157 (01) :294-323
[9]
Ventilator-induced lung injury upregulates and activates gelatinases and EMMPRIN - Attenuation by the synthetic matrix metalloproteinase inhibitor, Prinomastat (AG3340) [J].
Foda, HD ;
Rollo, EE ;
Drews, M ;
Conner, C ;
Appelt, K ;
Shalinsky, DR ;
Zucker, S .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2001, 25 (06) :717-724
[10]
Pulmonary surfactant: functions and molecular composition [J].
Goerke, J .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1998, 1408 (2-3) :79-89