Mechanical ventilation of isolated septic rat lungs: effects on surfactant and inflammatory cytokines (original) (raw)
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Effects of mechanical ventilation of isolated mouse lungs on surfactant and inflammatory cytokines
2001
Mechanical ventilation of the lung is an essential but potentially harmful therapeutic intervention for patients with acute respiratory distress syndrome. The objective of the current study was to establish and characterize an isolated mouse lung model to study the harmful effects of mechanical ventilation. Lungs were isolated from BalbC mice and randomized to either a nonventilated group, a conventionally ventilated group (tidal volume 7 mL. kg-1 , 4 cm positive endexpiratory pressure (PEEP)) or an injuriously ventilated group (20 mL. kg-1 , 0 cm PEEP). Lungs were subsequently analysed for lung compliance, morphology, surfactant composition and in¯ammatory cytokines. Injurious ventilation resulted in signi®cant lung dysfunction, which was associated with a signi®cant increase in pulmonary surfactant, and surfactant small aggregates compared to the other two groups. Injurious ventilation also led to a signi®cantly increased concentration of interleukin-6 and tumour necrosis factor-a in the lavage. It was concluded that the injurious effects of mechanical ventilation can effectively be studied in isolated mouse lung, which offers the potential of studying genetically altered animals. It was also concluded that in this model, the lung injury is, in part, mediated by the surfactant system and the release of in¯ammatory mediators.
Respiratory Physiology & Neurobiology, 2002
We investigated the potential inflammatory reaction induced by mechanical ventilation (MV) using 10 ml/kg tidal volume and no positive end-expiratory pressure (PEEP) in control (C, n= 8), spontaneously breathing (SB, n =12) and mechanically ventilated (MV, n= 12) rabbits with normal lungs. After 6 h (MV and SB groups) or immediately (C group), lungs were removed for measurement of wet-to-dry (W/D) weight ratio and for bronchoalveolar lavage (BAL). Pulmonary mechanics were also studied. MV animals developed a modest but significant (P B 0.01) impairment of arterial blood oxygenation and had higher W/D lung weight ratio than C ones. In MV group, BAL macrophage count was greater (PB0.05) than in SB one. MV induced an upregulation of MCP-1, TNF-a, and IL-1b gene transcription (mRNAs), without significant elevation of the corresponding protein cytokines in the BAL supernatant, except for MCP-1 (PB 0.05). These data suggest that MV, even using moderate tidal volume, elicits a pro-inflammatory stimulus to the lungs.
American Journal of Respiratory and Critical Care Medicine, 1999
Model-based neuro-fuzzy control of FiO 2 for intensive care mechanical ventilation HF Kwok, GH Mills, M Mahfouf, DA Linkens P3 Comparison of closed with open tracheal aspiration system A Sanver, A Topeli, Y Çetinkaya, S Kocagöz, S Ünal P4 A laboratory assessment of the learning and retention of skills required to use the Combitube and Laryngeal Mask Airway by non-anaesthetists C Coles, C Elding, M Mercer P5 Pediatric airway exchange catheter can be a lifesaving device for the adult patients who have risk factors for difficult tracheal reintubation L Dosemeci, F Gurpinar, M Yilmaz, A Ramazanoglu P6 Cricothyroidotomy for elective airway management in critically ill trauma patients SM Wanek, EB Gagnon, C Rehm, RJ Mullins P7 Comparison of two percutaneous tracheostomy techniques I . Ö Akinci, P Ozcan, S Tug v rul, N Çakar, F Esen, L Telci, K Akpir P8 Percutaneous tracheostomy in patients with ARDS on HFOV S Shah, M Read, P Morgan P9 The dilatational tracheotomy -minimally-invasive, bed-side, inexpensive -but safe? MG Baacke, I Roth, M Rothmund, L Gotzen P10 Combination stenting for central airway stenosis P11 Ulcerative laryngitis in children admitted to intensive care M Hatherill, Z Waggie, L Reynolds, A Argent P12 Bronchial asthma in intensive care department: the factors influencing on exacerbation severity TA Pertseva, KE Bogatskaya, KU Gashynova P13 Severe BOOP M Mer, R Taylor, GA Richards P14 Facial continuous positive airway pressure therapy for cardiogenic pulmonary oedema: a study of its efficacy in an emergency department setting within the UK C Read, P16 Noninvasive positive pressure ventilation in patients with blunt chest trauma and acute respiratory failure S Milanov, M Milanov P17 Helium-oxygen (He-O 2 ) enhances oxygenation and increases carbon dioxide clearance in mechanically ventilated patients JAS Ball, R Cusack, A Rhodes, RM Grounds P18 Optimal method of flow and volume monitoring in patients mechanically ventilated with helium-oxygen (He-O 2 ) mixtures JAS Ball, A Rhodes, RM Grounds P19 Lessons learned from airway pressure release ventilation LJ Kaplan, H Bailey P20 Patient controlled pressure support ventilation D Chiumello, P Taccone, L Civardi, E Calvi, M Mondino, N Bottino, P Caironi P21 Impact of weaning failure in the evolution of patients under mechanical ventilation A Bruhn, P22 Abstract withdrawn P23 Rapid reduction of oxygenation index by employment of a recruitment technique in patients with severe ARDS GA Richards, H White, M Hopley P24 The effects of recruitment maneuver on oxygenation in primary and secondary adult respiratory distress syndrome S Tug v rul, N Çakar, IÖ Akinci, P Ergin Özcan, M Tug v rul, F Esen, L Telci, K Akpir Contents Available online http://ccforum.com/supplements/5/S1 Critical Care Vol 5 Suppl 1 Contents P25 Comparison of the P/V curve obtained by the supersyringe and the optoelectronic plethysmography D Chiumello, E Calvi, E Noe', L Civardi, E Carlesso, A Aliverti, R Dellacà P26 Assessment of static compliance and estimated lung recruitment as a tool for PEEP setting in ARDS patients P Dostal, V Cerny, R Parizkova P27 Positive end-expiratory pressure does not increase intraocular pressure in patients with intracranial pathology K Kokkinis, P Manolopoulou, J Katsimpris, S Gartaganis P28 Effects of lung recruitment and PEEP after CPB on pressure-absolute volume curves T Dyhr, A Larsson P29 The histopathological changes comparison in healthy rabbit lung ventilated with ZEEP, Sigh and PEEP Ç Yardimci, G Meyanci, H Öz, I Paksoy
Effect of Mechanical Ventilation on Cytokine Response to Intratracheal Lipopolysaccharide
Anesthesiology, 2004
Background Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation. Methods Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP. Results In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein ...
Journal of Applied Physiology, 2007
Lung morpho-functional alterations and inflammatory response to various types of mechanical ventilation (MV) have been assessed in normal, anesthetized, open-chest rats. Measurements were taken during protective MV [tidal volume (Vt) = 8 ml/kg; positive end-expiratory pressure (PEEP) = 2.6 cmH2O] before and after a 2- to 2.5-h period of ventilation on PEEP (control group), zero EEP without (ZEEP group) or with administration of dioctylsodiumsulfosuccinate (ZEEP-DOSS group), on negative EEP (NEEP group), or with large Vt (26 ml/kg) on PEEP (Hi-Vt group). No change in lung mechanics occurred in the Control group. Relative to the initial period of MV on PEEP, airway resistance increased by 33 ± 4, 49 ± 9, 573 ± 84, and 13 ± 4%, and quasi-static elastance by 19 ± 3, 35 ± 7, 248 ± 12, and 20 ± 3% in the ZEEP, NEEP, ZEEP-DOSS, and Hi-Vt groups. Relative to Control, all groups ventilated from low lung volumes exhibited histologic signs of bronchiolar injury, more marked in the NEEP and ZEE...
Intensive Care Medicine, 2008
Objective: To describe the time course of the changes in pulmonary and vascular function, and systemic inflammation induced by injurious mechanical ventilation. Design: Experimental study in an animal model of ventilator-induced lung injury. Setting: Animal research laboratory. Methods: Anesthetized male adult Sprague-Dawley rats were ventilated with V T 9 ml/kg and PEEP 5 cm H 2 O, or V T 35 ml/kg and zero PEEP for 1 h, and were killed. Other rats received ventilation for 1 h with high V T , to observe survival (n = 36), or to be monitored and killed at different points in time (24, 72 and 168 h; n = 7 in each group). Blood samples for measuring biochemical parameters were obtained. Post-mortem, a bronchoalveolar lavage (BAL) was performed, the aorta and pulmonary microvessels were isolated to examine ex-vivo vascular responses and pulmonary slices were examined (light microscopy). Measurements and results: Mortality in rats ventilated with high V T was 19 of 36 (54%).
Histochemistry and Cell Biology, 2020
Mechanical ventilation triggers the manifestation of lung injury and pre-injured lungs are more susceptible. Ventilationinduced abnormalities of alveolar surfactant are involved in injury progression. The effects of mechanical ventilation on the surfactant system might be different in healthy compared to pre-injured lungs. In the present study, we investigated the effects of different positive end-expiratory pressure (PEEP) ventilations on the structure of the blood-gas barrier, the ultrastructure of alveolar epithelial type II (AE2) cells and the intracellular surfactant pool (= lamellar bodies, LB). Rats were randomized into bleomycin-pre-injured or healthy control groups. One day later, rats were either not ventilated, or ventilated with PEEP = 1 or 5 cmH 2 O and a tidal volume of 10 ml/kg bodyweight for 3 h. Left lungs were subjected to design-based stereology, right lungs to measurements of surfactant proteins (SP−) B and C expression. In pre-injured lungs without ventilation, the expression of SP-C was reduced by bleomycin; while, there were fewer and larger LB compared to healthy lungs. PEEP = 1 cmH 2 O ventilation of bleomycin-injured lungs was linked with the thickest blood-gas barrier due to increased septal interstitial volumes. In healthy lungs, increasing PEEP levels reduced mean AE2 cell size and volume of LB per AE2 cell; while in pre-injured lungs, volumes of AE2 cells and LB per cell remained stable across PEEPs. Instead, in pre-injured lungs, increasing PEEP levels increased the number and decreased the mean size of LB. In conclusion, mechanical ventilation-induced alterations in LB ultrastructure differ between healthy and pre-injured lungs. PEEP = 1 cmH 2 O but not PEEP = 5 cmH 2 O ventilation aggravated septal interstitial abnormalities after bleomycin challenge.
Pediatric Pulmonology, 2011
Objectives-To test the hypothesis that surfactant, when given prophylactically during one lung ventilation, improves physiological stability and reduces inflammation. Methods-Prospective controlled animal study. After 30 minutes of mechanical ventilation, surfactant was administered to the left lung of the treatment group. Right lung mechanical ventilation continued for 3 hours, after which the left lung was unblocked. Bilateral mechanical ventilation was continued for 30 minutes thereafter. Physiological parameters and biomarkers of inflammation in plasma, lung tissue homogenates, and bronchoalveolar lavage were measured. Measurements and Main Results-Oxygenation improved in the surfactant group, reaching statistical significance at 3 hours of one lung ventilation and again after 30 minutes of bilateral mechanical ventilation following the one lung ventilation. Plasma levels of interleukin-1 β, interleukin-6, and tumor necrosis factor-α showed a trend for reduction. The lung homogenates from the ventilated lungs had significantly lower levels of interleukin-1 β (P < 0.01) and interleukin-6 (P < 0.01). The bronchoalveolar lavage specimen showed an overall reduction in the cytokine levels; interleukin-1 β was significantly lower in the ventilated lungs (P < 0.01). Conclusions-Surfactant administration improves oxygenation and decreases inflammation, as evidenced by a decrease in several inflammatory cytokines both in the plasma and lungs of a piglet model of one lung ventilation.
Ventilation with high tidal volume induces inflammatory lung injury
Brazilian Journal of Medical and Biological Research, 2002
Mechanical ventilation with high tidal volumes (V T) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH 2 O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO 2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-α concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-α concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-α in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response.