Surfactant administration prior to one lung ventilation: Physiological and inflammatory correlates in a piglet model (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.
Journal of Applied Physiology, 2001
Mechanical ventilation of isolated septic rat lungs: effects on surfactant and inflammatory cytokines. J Appl Physiol 91: 811-820, 2001.-The effects of mechanical ventilation (MV) on the surfactant system and cytokine secretion were studied in isolated septic rat lungs. At 23 h after sham surgery or induction of sepsis by cecal ligation and perforation (CLP), lungs were excised and randomized to one of three groups: 1) a nonventilated group, 2) a group subjected to 1 h of noninjurious MV (tidal volume ϭ 10 ml/kg, positive end-expiratory pressure ϭ 3 cmH 2O), or 3) a group subjected to 1 h of injurious MV (tidal volume ϭ 20 ml/kg, positive end-expiratory pressure ϭ 0 cmH 2O). Nonventilated sham and CLP lungs had similar compliance, normal lung morphology, surfactant, and cytokine concentrations. Injurious ventilation decreased compliance, altered surfactant, increased cytokines, and induced morphological changes compared with nonventilation in sham and CLP lungs. In these lungs, the surfactant system was similar in sham and CLP lungs; however, tumor necrosis factor-␣ and interleukin-6 levels were significantly higher in CLP lungs. We conclude that injurious ventilation altered surfactant independent of sepsis and that the CLP lungs were predisposed to the secretion of larger amounts of cytokines because of ventilation.
Effect of ventilation strategy and surfactant on inflammation in experimental pneumonia
European Respiratory Journal, 2005
This study explored, the inflammatory response during experimental pneumonia in surfactant-depleted animals as a function of ventilation strategies and surfactant treatment. Following intratracheal instillation of Group B streptococci (GBS), surfactant-depleted piglets were treated with conventional (positive-end expiratory pressure (PEEP) of 5 cmH 2 O, tidal volume 7 mL?kg-1) or open lung ventilation. During the latter, collapsed alveoli were recruited by applying high peak inspiratory pressures for a short period of time, combined with high levels of PEEP and the smallest possible pressure amplitude. Subgroups in both ventilation arms also received exogenous surfactant. Conventionally ventilated healthy animals receiving GBS and surfactantdepleted animals receiving saline served as controls. In contrast with both control groups, surfactant-depleted animals challenged with GBS and conventional ventilation showed high levels of interleukin (IL)-8, tumour necrosis factor (TNF)-a and myeloperoxidase in bronchoalveolar lavage fluid after 5 h of ventilation. Open lung ventilation attenuated this inflammatory response, but exogenous surfactant did not. Systemic dissemination of the inflammatory response was minimal, as indicated by low serum levels of IL-8 and TNF-a. In conclusion, the current study indicates that the ventilation strategy, but not exogenous surfactant, is an important modulator of the inflammation during Group B streptococci pneumonia in mechanically ventilated surfactant-depleted animals.
Pulmonary surfactant is altered during mechanical ventilation of isolated rat lung
Critical Care Medicine, 2000
Objective: To test the hypothesis that the lung injury induced by certain mechanical ventilation strategies is associated with changes in the pulmonary surfactant system. Design: Analysis of the pulmonary surfactant system from isolated rat lungs after one of four different ventilatory strategies. Setting: A research laboratory at a university. Subjects: A total of 45 Sprague-Dawley rats. Interventions: Isolated lungs were randomized to either no ventilation (O-TIME) or to ventilation at 40 breaths/min in a humidified 37°C chamber for either 30 mins or 120 mins with one of the following four strategies: a) control (CON, 7 mL/kg, 3 cm H 2 O positive end-expiratory pressure); b) medium volume, zero end-expiratory pressure (MVZP, 15 mL/kg, O cm H 2 O end-expiratory pressure); c) medium volume, high positive end-expiratory pressure (MVHP, 15 mL/kg, 9 cm H 2 O positive end-expiratory pressure); and d) high volume, zero end-expiratory pressure (HVZP, 40 mL/kg, 0 cm H 2 O end-expiratory pressure). Measurements: Pressure-volume curves were determined before and after the ventilation period, after which the lungs were lavaged for surfactant analysis. Main Results: Compared with 0-TIME, 30 mins of ventilation with the HVZP strategy or 120 mins of ventilation with CON and MVZP strategies caused a significant decrease in compliance. Groups showing a decreased compliance had significant increases in the amount of surfactant, surfactant large aggregates, and total lavage protein compared with 0-TIME. Conclusions: A short period of injurious mechanical ventilation can cause a decrease in lung compliance that is associated with a large influx of proteins into the alveolar space and with alterations of the pulmonary surfactant system. The changes of surfactant in these experiments are different from those seen in acute lung injury, indicating that they may represent an initial response to mechanical ventilation.
Mechanisms of ventilation-induced lung injury : role of surfactant
1999
Background: Intclmittent positive pressure ventilation with high peak inspiratory lung volumes (HIPPV) has been shown to induce pulmonary edema and surfactant changes. \Ve tested the effect of exogenous surfactant preceding HIPPV on lung function and permeability. Methods: Five groups of6 Sprague-Dawley rats received intratracheal administration of saline or 50, 100 or 200 mg/kg surfactant or no intra-tracheal administration prior to 20 min of HIPPV. Gas exchange was measured. A sixth group served as non-treated, non-ventilated controls. Post-mortem static pressure-volume curves and total lung volume at 5 cmH 2 0 transpulmonary pressure (Vs) were recorded; Gruenwald index and the steepest part of the compliance curve (Crna.;:) were calculated. Active and non-active total phosphorus and minimal surface tension (Ymin) ofbroncho-alveolar lavage (BAL) were measured. In another experiment in 5 groups of 6 rats, Evans blue lung penneability was measured. Four groups received 100, 200 or 400 mg/kg surfactant intra-tracheally or no intra-tracheal administration prior to 20 min HIPPY. A fifth group served as non-treated, non-ventilated controls. Results: Most active phosphorus was recovered in the group that received 200 mg/kg surfactant. This dose preserved Y s , Cmax, Gruenwald index and oxygenation after 20 min HIPPV and reduced Ym' " of BAL to control valuc; 200 and 400 mg/kg surfactant reduced Evans blue permeability. Conclusions: Exogenous surfactant preceding HIPPV prevents impainnent of oxygenation, lung mechanics and minimal surface tension of BAL fluid and reduces Evans blue pemleability. These data indicate a beneficial effect of surfactant on ventilation-induced lung injury.
British Journal of Anaesthesia, 2001
A combination of exogenous surfactant and partial liquid ventilation (PLV) with per¯uorocarbons should enhance gas exchange, improve respiratory mechanics and reduce tissue damage of the lung in acute lung injury (ALI). We used a small dose of exogenous surfactant with and without PLV in an experimental model of ALI and studied the effects on gas exchange, haemodynamics, lung mechanics, and lung pathology. ALI was induced by repeated lavages (Pa O 2 /FI O 2 less than 13 kPa) in 24 anaesthesized, tracheotomized and mechanically ventilated (FI O 2 1.0) juvenile pigs. They were treated randomly with either a single intratracheal dose of surfactant (50 mg kg ±1 , Curosurf â , Serono AG, Mu Ènchen, Germany) (SURF-group, n=8), a single intratracheal dose of surfactant (50 mg kg ±1 , Curosurf â ) followed by PLV with 30 ml kg ±1 of per¯uorocarbon (PF 5080, 3M, Germany) (SURF-PLV-group, n=8) or no further intervention (controls, n=8). Pulmonary gas exchange, respiratory mechanics, and haemodynamics were measured hourly for a 6 h period. In the SURF-group, the intrapulmonary right-to-left shunt (Q Ç S/Q Ç T) decreased signi®cantly from mean 51 (SEM 5)% after lavage to 12 (2)%, and Pa O 2 increased sig-ni®cantly from 8.1 (0.7) to 61.2 (4.7) kPa compared with controls and compared with the SURF-PLV-group (P<0.05). In the SURF-PLV-group, Q Ç S/Q Ç T decreased signi®cantly from 54 (3)% after induction of ALI to 26 (3)% and Pa O 2 increased signi®cantly from 7.2 (0.5) to 30.8 (5.0) kPa compared with controls (P<0.05). Static compliance of the respiratory system (C RS ), sig-ni®cantly improved in the SURF-PLV-group compared with controls (P<0.05). Upon histological examination, the SURF-group revealed the lowest total injury score compared with controls and the SURF-PLV-group (P<0.05). We conclude that in this experimental model of ALI, treatment with a small dose of exogenous surfactant improves pulmonary gas exchange and reduces the lung injury more effectively than the combined treatment of a small dose of exogenous surfactant and PLV.
Journal of Anesthesia & Clinical Research, 2014
Study objective: The purpose of this study was to investigate if spontaneous one-lung ventilation would induce any type of inflammatory lung response when compared to spontaneous two-lung ventilation and its intensity, by quantification of inflammatory cells in lung histology at the end of the procedure. Design: In vivo prospective randomised animal study Setting: University research laboratory Subjects: New Zealand rabbits Interventions: Rabbits (n=20) were randomly assigned to 4 groups (n=5 each group). Groups 1 and 2 were submitted to one-lung ventilation, during 20 and 75 minutes respectively; groups 3 and 4 were submitted to two-lung ventilation during 20 and 75 minutes and considered controls. Ketamine/xylazine was administered for induction and maintenance of anesthesia. One-lung ventilation was achieved by administration of air into the interpleural space, and left lung collapse was visually confirmed through the centre of the diaphragm. Measurements: Lung histology preparations were observed under light microscopy for quantification of the inflammatory response (light, moderate and severe). Main results: All subjects had at least light inflammatory response. However, rabbits submitted to one-lung ventilation had a statistically significant value for the occurrence of moderate inflammation (p<0.05). The inflammatory response found included mainly eosinophils, with an average proportion of 75/25 to other polymorphonuclear cells. No differences between groups were found regarding gas exchange, heart rate and respiratory rate. Conclusions: In this spontaneous one-lung ventilation model, lung collapse was positively associated with a greater inflammatory response when compared to normal two-lung ventilation.
Intensive Care Medicine, 2002
Objective: To determine the effect of pretreatment with exogenous surfactant on ventilatorinduced decompartmentalization of TNF-α. Design and setting: Prospective, randomized, animal study in the experimental laboratory of a university. Subjects and interventions: Male Sprague-Dawley rats (n=102) received lipopolysaccharide either intratracheally or intraperitoneally to stimulate TNF-α production; onehalf of the animals were pretreated with surfactant. Animals were ventilated for 20 min with a peak inspiratory pressure/positive end-expiratory pressure (PEEP) ratio of either 45/0 or 45/10 (frequency 30 bpm, I/E ratio 1:2, FIO 2 =1). Measurements and results: Blood gas tension and arterial pressures were recorded 1, 10, and 20 min after the start of mechanical ventilation. After the animals were killed pressure-volume curves were recorded, and bronchoalveolar lavage was performed for assessment of protein content and the small/large surfactant aggregate ratio. TNF-α was determined in serum and bronchoalveolar lavage. Pretreatment with surfactant decreased decompartmentalization of TNF-α during 45/0 ventilation. Addition of a PEEP level of 10 cm H 2 O reduced decompartmentalization even further. In addition, surfactant prevented deterioration in oxygenation and decreased accumulation of protein in the bronchoalveolar lavage in the zero-PEEP group. Conclusions: An excess of active surfactant decreases transfer of cytokines across the alveolar-capillary membrane similar to PEEP. The combination of PEEP and surfactant reduces decompartmentalization of TNF-α even further.
Treatment of ventilation-induced lung injury with exogenous surfactant
Intensive Care Medicine, 2001
tory rate of 40 bpm. One group received a bolus of surfactant and the other group received no treatment. Measurements and results: Blood gas tension and arterial blood pressures were recorded every 30 min for 2 h. After the study period, a pressurevolume curve was recorded. Then, a broncho-alveolar lavage (BAL) was performed to determine protein content, minimal surface tension, and surfactant composition in the BAL fluid. Oxygenation, lung mechanics, surfactant function and composition were significantly improved in the surfactant-treated group compared to the ventilated and non-ventilated control groups. Conclusion: We conclude that exogenous surfactant can be used to treat VILI.