Decrease in Lung Volume Depends on End-Expiratory Pressure in a Rabbit Model of Airway Lavage

Krause, Martín; Hoehn, Thomas

doi:10.1159/000029387

Cited by 12 publications

(5 citation statements)

References 28 publications

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“…After the first lavage, positive end-expiratory pressure was increased to 8 cm H 2 O to speed up surfactant removal and alveolar collapse, which varies according to the positive end-expiratory pressure level chosen (25), and the ventilatory rate was switched to 45 breaths/min to ensure adequate ventilation. During the first 6 lavages, the piglets were alternately positioned on their left and right sides.…”

Section: Methodsmentioning

confidence: 99%

Topical inhibition of nuclear factor-κB enhances reduction in lung edema by surfactant in a piglet model of airway lavage

Ankermann

Reisner²,

Wiemann³

et al. 2005

Critical Care Medicine

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Section: Methodsmentioning

confidence: 99%

Topical inhibition of nuclear factor-κB enhances reduction in lung edema by surfactant in a piglet model of airway lavage

Ankermann

Reisner²,

Wiemann³

et al. 2005

Critical Care Medicine

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“…Each lavage involved the instillation and removal of 35 mL/kg of warmed normal saline via the ETT carried out over a 30-s period. After the first lavage, PEEP was increased to 0.8 kPa and the ventilator rate to 60 breaths/min to ensure adequate oxygenation and ventilation and to hasten surfactant removal and alveolar collapse (15). The first six lavages were performed in changing side positions.…”

Section: Methodsmentioning

confidence: 99%

Alveolar Recruitment Promotes Homogeneous Surfactant Distribution in a Piglet Model of Lung Injury

et al. 2001

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Uneven distribution of exogenous surfactant contributes to a poor clinical response in animal models of respiratory distress syndrome. Alveolar recruitment at the time of surfactant administration may lead to more homogeneous distribution within the lungs and result in a superior clinical response. To investigate the effects of three different volume recruitment maneuvers on gas exchange, lung function, and homogeneity of surfactant distribution, we studied 35 newborn piglets made surfactant deficient by repeated airway lavage with warm saline. Volume recruitment was achieved by either a temporal increase in tidal volume or an increase in end-expiratory pressure during surfactant administration, yielding an increase in dynamic compliance of the respiratory system of 77% in the first group and an increase in functional residual capacity of 108% in the second group. A third group of piglets (all n ϭ 7) received a combination of both volume recruitment maneuvers, with increases in dynamic compliance of the respiratory system of 100% and in functional residual capacity of 192%. Those animals subjected to increased tidal volume showed an improved surfactant response in terms of oxygenation, ventilation, lung volumes, lung mechanics, and homogeneity of surfactant distribution. Increased end-expiratory volume augmented the surfactant effect only to some extent. The combination of both volume recruitment maneuvers, however, needed lung volumes beyond total lung capacity (approximately 56 mL/kg), thus probably inducing early sequelae of ventilatorinduced lung injury. We conclude that volume recruitment by means of increased tidal volumes at the time of surfactant administration leads to a superior surfactant effect owing to more homogeneous surfactant distribution within a collapsed lung. Surfactant treatment has reduced mortality and morbidity in infants with RDS (1). However, detrimental factors affecting response to therapy are numerous, such as uneven distribution of exogenous surfactant, insufficient dosage, inability of exogenous surfactant to enter the metabolic pathways, inhibition of surface activity by plasma-derived proteins, or respiratory failure caused by factors other than surfactant deficiency (2).Two clinical studies (3, 4) have identified patent ductus arteriosus, gas accumulation outside the alveolar level, and pulmonary infection as the main reasons for nonresponse in neonates with RDS, leading to an increased mortality as high as 40% of affected infants. Poor response, however, is thought to be predominantly caused by uneven surfactant distribution. Animal studies have shown that the distribution of exogenous surfactant is often nonuniform, and that nonuniform distribution patterns are associated with poor clinical response (5-7).The immediate increase in FRC after surfactant administration to infants with RDS (8 -10) can be considered to be the result of two mechanisms: stabilization of previously collapsing alveoli at end-expiration, and stabilization of alveoli already being ventilated at higher e...

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“…The ventilator was disconnected and 20 ml/kg of warmed 0.9 % saline was instilled into the trachea through a suction catheter. This volume represents the typical functional residual capacity of a healthy rabbit [13,14,15]. The ventilator was then re-connected and the inspiratory pressure was increased to maintain tidal volume at around 10 ml/kg (maximum airway pressure 24 cmH 2 O).…”

Section: Methodsmentioning

confidence: 99%

Randomised comparison of partial liquid ventilation, nebulised perfluorocarbon, porcine surfactant, artificial surfactant, and combined treatments on oxygenation, lung mechanics, and survival in rabbits after saline lung lavage

2000

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Decrease in Lung Volume Depends on End-Expiratory Pressure in a Rabbit Model of Airway Lavage

Cited by 12 publications

References 28 publications

Topical inhibition of nuclear factor-κB enhances reduction in lung edema by surfactant in a piglet model of airway lavage

Topical inhibition of nuclear factor-κB enhances reduction in lung edema by surfactant in a piglet model of airway lavage

Alveolar Recruitment Promotes Homogeneous Surfactant Distribution in a Piglet Model of Lung Injury

Randomised comparison of partial liquid ventilation, nebulised perfluorocarbon, porcine surfactant, artificial surfactant, and combined treatments on oxygenation, lung mechanics, and survival in rabbits after saline lung lavage

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