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Short-Term Exposure to High-Pressure Ventilation Leads to Pulmonary Biotrauma and Systemic Inflammation in the Rat

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Short-Term Exposure to High-Pressure Ventilation Leads to Pulmonary Biotrauma and Systemic Inflammation in the Rat 513-519 3/3/08 15:18 Page 513 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 21: 513-519, 2008 513 Short-term exposure to high-pressure ventilation leads to pulmonary biotrauma and systemic inflammation in the rat SANDRA HOEGL1,3, KIM A. BOOST2, MICHAEL FLONDOR2, PATRICK SCHEIERMANN2, HEIKO MUHL3, JOSEF PFEILSCHIFTER3, BERNHARD ZWISSLER1 and CHRISTIAN HOFSTETTER2 1Clinic of Anaesthesiology, University Hospital of Ludwig-Maximilians-University, Marchioninistrasse 15, D-81377 Munich; 2Clinic of Anaesthesiology, 3Pharmazentrum Frankfurt/ZAFES, University Hospital of Johann Wolfgang Goethe-University, Theodor-Stern-Kai 7, D-60590 Frankfurt/Main, Germany Received November 9, 2007; Accepted December 21, 2007 Abstract. Though often lifesaving, mechanical ventilation Introduction itself bears the risk of lung damage [ventilator-induced lung injury (VILI)]. The underlying molecular mechanisms have The application of mechanical ventilation is a key factor in not been fully elucidated, but stress-induced mediators seem the treatment of critically ill patients. However, mechanical to play an important role in biotrauma related to VILI. Our ventilation itself can cause adverse effects on lung paren- purpose was to evaluate an animal model of VILI that allows chyma and gas exchange, resulting in ventilator-induced lung the observation of pathophysiologic changes along with injury (VILI). In patients with severe respiratory failure in parameters of biotrauma. For VILI induction, rats (n=16) particular, high airway pressures can aggravate structural were ventilated with a peak airway pressure (pmax) of 45 cm lung damage and increase systemic cytokine levels and H2O and end-expiratory pressure (PEEP) of 0 for 20 min, mortality rates (1). followed by an observation time of 4 h. In the control group To further improve the outcome of critically ill patients, a better understanding of the detrimental mechanisms of VILI (n=8) the animals were ventilated with a pmax of 20 cm H2O and PEEP of 4. High-pressure ventilation resulted in an is therefore required. In 1974, Webb and Tierney were the first to demonstrate that high peak airway pressures result in increase in paCO2 and a decrease in paO2 and mean arterial pressure. Only 4 animals out of 16 survived 4 h and VILI lung oedema, alveolar disruption, capillary leakage and death lungs showed severe macroscopic and microscopic damage, (2). In addition to this direct lung damage by volu- and/or oedema and neutrophil influx. High-pressure ventilation barotrauma, studies performed subsequently highlighted the increased the cytokine levels of macrophage inflammatory significance of local inflammation and lung-borne cytokines protein-2 and IL-1ß in bronchoalveolar lavage and plasma. (biotrauma). This inflammatory reaction is not confined to VILI also induced pulmonary heat shock protein-70 the lungs but also extends to systemic circulation, thus expression and the activity of matrix metalloproteinases. The contributing to the development of systemic inflammatory animal model used enabled us to observe the effect of high- response (SIRS) and multiple organ dysfunction syndrome pressure ventilation on mortality, lung damage/function and (MODS) (3). biotrauma. Thus, by combining barotrauma with biotrauma, However, the role of proinflammatory mediators in the this animal model may be suitable for studying therapeutical course of VILI is still controversial, as several in vitro and approaches to VILI. in vivo models of VILI have shown inconsistencies in cytokine response (4). Most studies focusing on cytokine release during VILI were performed in pre-damaged lungs. In these so-called ‘two-hit models’, in addition to mechanical _________________________________________ injury the animals were exposed to surfactant depletion (5), hyperoxia (6) or endotoxemia (7). Correspondence to: Dr Sandra Hoegl, Clinic of Anaesthesiology, Therefore, in order to isolate the specific inflammatory University Hospital of Ludwig-Maximilians-University, effects of mechanical stress, we established an animal model Marchioninistrasse 15, D-81377 Munich, Germany of ventilator-induced lung injury in previously healthy rats. E-mail: [email protected] In addition to the pathophysiologic changes in terms of barotrauma, we aimed to characterize the local and systemic Key words: biotrauma, mechanical ventilation, ventilator-induced inflammatory response to VILI in terms of biotrauma. For lung injury the investigation of possible therapeutic agents, an animal model of VILI that allows the simultaneous observation of local and systemic inflammation, impairment of lung structure and function and, above all, systemic alterations and mortality is of special interest. 513-519 3/3/08 15:18 Page 514 514 HOEGL et al: VILI LEADS TO BIOTRAUMA AND SYSTEMIC INFLAMMATION Materials and methods ventral and dorsal surface into upper and lower halves and the presence and extent of haemorrhage was examined. When Animal preparation. All animal experiments were approved more than half of the lung surface showed haemorrhage this by the governmental board for the care and use of animal was correlated with a score of 2, less than half with a score of subjects (Regierungspraesidium Darmstadt, Germany) and 1 and no visible severe lung damage with a score of 0. This performed according to the ‘Guide for the Care and Use of resulted in a lung injury score from 0 (uninjured lung) to 16 Laboratory Animals’, National Academic Press, Washington (maximal lung damage). D.C., 1996. Male Sprague-Dawley rats (n=24) were obtained from Janvier (Le Genest-St-Isle, France; mean body weight ± Isolation of BAL cells, BALF and lung tissue. The broncho- SD, 600±30 g). Rats were anesthetized initially by i.p. alveolar lavage fluid obtained was centrifuged and the injection of pentobarbital (Narcoren, Merial, Halbergmoos, supernatant (BALF) was frozen and stored at -80˚C. The cell Germany; 50 mg/kg) and fentanyl (Janssen-Cilag, Neuss, suspension was used for a differential cell count according to Germany; 0.05 mg/kg), weighed and then placed supine on a morphologic criteria in cytocentrifuged smears stained with heating pad. Animals were tracheotomised and ventilated May-Gruenwald-Giemsa. To analyze nitrite release as a read- with an infant ventilator (Stephanie®, Stephan, Gackenbach, out for inducible nitric oxide synthase (iNOS) activation, Germany) using pressure controlled ventilation, with the cells were seeded on polystyrene plates, and after initial following ventilator adjustments as the standard: peak airway cultivation for 2 h non-adherent cells were removed by pressure (pmax), 20 cm H2O; end-expiratory pressure (PEEP), washing. Adherent cells were regarded as alveolar macro- 4 cm H2O; f, 30/min; fraction of inspired oxygen (FiO2), 0.21; phages and incubated at 37˚C in 5% CO2 for 20 h. Nitrite inspiratory to expiratory time ratio (I:E), 1:2. A temperature concentrations in cell culture supernatants were determined probe was inserted rectally for the continuous monitoring of by Griess assay (10). body temperature in order to keep it constant at 37.0-38.0˚C For Western blotting, lung samples were homogenized throughout the experiment. Fluid-filled polyurethane in lysis buffer (150 mM NaCl, 1 mM CaCl2, 25 mM TrisCl, catheters (ID, 0.58 mm; OD 0.96, mm; SIMS Portex Ltd, pH 7.4, 1% Triton X-100), supplemented with protease Hythe, UK) were inserted in the right femoral vein and artery inhibitor cocktail (Roche Diagnostics, Mannheim, Germany), for the infusion of anaesthetics and blood gas analysis, DTT, Na3VO4, PMSF (each 1 mM) and NaF (20 mM). The respectively. Anaesthesia was maintained by the continuous tissue extract was cleared by centrifugation and the super- i.v. infusion of pentobarbital (5-10 mg/kg/h) and fentanyl natant was frozen and stored at -80˚C. Total protein (2.5-5.0 μg/kg/h). concentrations of BALF samples and lung homogenates were determined with the Bradford assay (11). Experimental groups. After a stabilization period of 15 min, rats were randomly assigned either to the injurious Plasma samples and ELISA assay. The blood samples were mechanical ventilation group (highP; n=16) or the control centrifuged and the resulting plasma was collected and group (lowP; n=8). For the induction of VILI in the highP frozen at -80˚C. The BALF and plasma levels of macrophage group, the ventilator setting was changed for 20 min to a inflammatory protein-(MIP)-2 (Biosource, Camarillo, CA) and pmax of 45 cm H2O, PEEP of 0 cm H2O and I:E of 1:1, and IL-1ß (R&D Systems, Wiesbaden, Germany) were determined afterwards reset to the standard ventilator adjustments. The by ELISA according to the manufacturer's instructions. control group (lowP) was ventilated with standard ventilator adjustments for the observation time of 4 h. Western blot analysis and SDS-PAGE zymography. Western Rats were monitored for 4 h and hourly blood gas blot analysis of heat shock protein (HSP)-70 (StressGen, Ann analyses were performed. At the end of the protocol animals Arbor, MI) in lung homogenates was performed using were exsanguinated and blood samples were obtained. After standard procedures. thoracotomy and inspection of the lung the accessory lobe Gelatinolytic activity of proteins from BALF (30 μl) was was ligated and the rest of the lung was lavaged with PBS assessed as described previously (12). Gelatinolytic activity (Serva, Heidelberg, Germany). Subsequently, the accessory of proteins was visualized as lightened areas on an otherwise lobe was cut into three parts, one part was fixed in 10% blue gel and their migration properties were determined by buffered formalin for histologic examination and the other comparison with prestained full-range rainbow protein two were snap-frozen in liquid nitrogen and stored at -80˚C. markers (Amersham Pharmacia Biotech, Freiburg, Germany). This study focused on the evolving inflammatory processes. Therefore, no plasma, bronchoalveolar lavage Statistics. Data are presented as median ± semi-interquartile (BAL) or lung probes were harvested in animals that died range (IQR). Survival in the two study groups was compared before the critical time period of 2 h after the induction of using a log-rank test and differences between the groups VILI.
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