Surfactant Treatment Effects on Lung Structure and Type II Cells of Preterm Ventilated Lambs

Pinkerton, Kent E.; Ikegami, Machiko; Dillard, Lisa M.; Jobe, Alan H.

doi:10.1159/000014223

Cited by 12 publications

(4 citation statements)

References 31 publications

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“…This is supported by the finding of an almost double risk of BPD in the group exposed to beta-methasone when birth weight and degree of prematurity are taken into account. The lack of association between the use of pulmonary surfactant with the development of BPD found in this study has been shown by others [9,26,27] but it is interesting to see that the more severe form of BPD was reduced in favor of milder disease with its use.…”

Section: Impact Of Use Of Antenatal Corticosteroids and Pulmonary Surfactantsupporting

confidence: 58%

The Long-term Impacts of Birth Weight and Respiratory Complications after a Preterm Birth

Jennifer

Ry²,

Zysman-Colman³

et al. 2014

J Neonatal Biol

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Background: Infant respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) remain important respiratory complications of preterm births. This study aims at establishing the incidence and impact of respiratory complications and extreme low birth weight (ELBW) on the healthcare utilization of a population of preterm infants.Methods: Retrospective cohort study using administrative healthcare databases of the province of Quebec (Canada). The main outcome measures of healthcare utilization, hospital admissions, hospital mortality and use of prescription drugs were studied in 55 033 subjects born prematurely with or without respiratory complications such as BPD or RDS between 1999 and 2009.Results: Preterm infants with BPD and RDS had significantly higher hospital readmissions per person-year. This trend persisted for the entire duration of the 10-year follow-up. Diagnoses of childhood asthma, attention deficit hyperactivity disorder and cerebral palsy were more frequent in BPD subjects, but were not influenced by birth weight. Extreme low birth weight carried odds ratio of 38.0 [33.5, 43.2] and 3.5 [3.2, 3.9] respectively for the occurrence of BPD and RDS, and was associated with greater mortality, longer hospital stay and more medical visits per person-year. Except for anxiolytics and sedatives, bronchopulmonary dysplasia subjects were not more likely to have been prescribed neurological and psychiatric medications.Conclusions: Birth weight is a major determinant in the occurrence of respiratory complications following a preterm birth. The impacts of BPD and extreme low birth weight following a preterm birth have lasting consequences on respiratory health and healthcare utilization.

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Section: Impact Of Use Of Antenatal Corticosteroids and Pulmonary Surfactantsupporting

confidence: 58%

The Long-term Impacts of Birth Weight and Respiratory Complications after a Preterm Birth

Jennifer

Ry²,

Zysman-Colman³

et al. 2014

J Neonatal Biol

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“…The high PIP of up to 40-50 cmH 2 O for the first 15 min were needed to clear the airways of fluid. Ventilation without surfactant results in over distention of the open lung because of the non-uniform surface tensions throughout the lung (32). …”

Section: Discussionmentioning

confidence: 99%

Positive End-Expiratory Pressure and Tidal Volume During Initial Ventilation of Preterm Lambs

et al. 2008

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Positive end-expiratory pressure (PEEP) protects the lung from injury during sustained ventilation, but its role in protecting the lung from injury during the initiation of ventilation in the delivery room is not established. We aimed to evaluate whether PEEP and/or tidal volume (V T ) within the first 15-min of ventilation are protective against lung injury. Operatively delivered preterm lambs (133 Ϯ 1 d gestation) were randomly assigned to unventilated controls or to one of four 15 min ventilation interventions: 1) V T 15 mL/kg, PEEP 0 cm H 2 O; 2) V T 15 mL/kg, PEEP 5 cm H 2 O; 3) V T 8 mL/kg, PEEP 0 cm H 2 O; and 4) V T 8 mL/kg, PEEP 5 cm H 2 O. Each group was subsequently ventilated with V T Ͻ10 mL/kg, PEEP 5 cm H 2 O for 1 h 45 min. Lung function was assessed and measurements of lung injury were evaluated postmortem. After the 15 min ventilation maneuver, the V T 15 groups were hypocarbic, had higher oxygenation, and required lower pressures than the V T 8 groups; no consistent effect of PEEP was found. Markers of lung injury were significantly elevated in all ventilation groups compared with unventilated controls; no effect of PEEP was found. Ventilation resulted in localization of IL-6 to the small airways. Initial ventilation of preterm lambs with PEEP and/or V T of 8 mL/kg did not prevent an inflammatory injury to the lung. T he initiation of breathing at birth is an essential but complex adaptation that must rapidly transition the fluid filled fetal lung to gas exchange (1). Critical components of this transition are clearance of fluid from the airways, establishment of a functional residual capacity (FRC), and increased blood flow to the lungs. This transition often requires assistance for term infants and is more difficult and ineffective for preterm infants. A poor transition to air breathing in preterm infants is frequently because of surfactant deficiency, decreased respiratory drive, and perhaps more lung fluid as the majority of preterm infants are now delivered via cesarean section (2). Despite the frequent need for ventilatory assistance after delivery, and numerous experimental demonstrations that the preterm lung can be easily injured by mechanical ventilation (3,4), there is minimal clinical information about how best to provide initial ventilatory assistance to the preterm lung. The equipment used for resuscitation of the preterm has not been standardized and does not allow for accurate control of tidal volume (V T ), positive end-expiratory pressure/ continuous positive airway pressure (PEEP/CPAP), or inspiratory times (5,6).Ventilation of the preterm lung for hours without PEEP will cause lung injury and high initial V T s further increase that lung injury (3,4,7). A brief period of high V T ventilation without PEEP will injure the preterm lung and subsequent ventilation with PEEP will amplify that injury (8); this injury can be reduced by surfactant treatment before mechanical ventilation of the preterm lung (4,9). In preterm sheep and baboons, CPAP decreases injury compared ...

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“…The preterm sheep lung at 130 d GA also is very surfactant deficient, and ventilation of the surfactant-deficient preterm lung causes nonuniform inflammation characterized by overinflation adjacent to regions of atelectasis (10). We treated the lambs with surfactant to minimize regional overdistention and to permit ventilation with lower pressures.…”

Section: Discussionmentioning

confidence: 99%

“…The preterm fetal lung does not have increased permeability to protein relative to the mature lung (9). Therefore, the increased permeability that occurs in ventilated preterm lungs is thought to result from the effects of nonuniform inflation on a structurally immature and surfactant-deficient lung that contains insufficient collagen and elastin (10,11). The immature lung also has decreased host defense surfactant protein (SP)-A and SP-D and has immature immune systems with depressed second messenger responses making it potentially more susceptible to endotoxin-induced injury (12,13).…”

mentioning

confidence: 99%

Intratracheal Endotoxin Causes Systemic Inflammation in Ventilated Preterm Lambs

Kramer

Ikegami²,

Jobe³

2002

Am J Respir Crit Care Med

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Intratracheal endotoxin causes acute inflammation in the adult lung, and injurious styles of mechanical ventilation can result in systemic inflammation derived from the lungs. We asked how ventilated premature and near-term lungs responded to intratracheal endotoxin and if systemic inflammation occurred. Lambs delivered at 130 d gestational age (GA) were treated with surfactant or surfactant plus endotoxin (0.1 mg/kg or 10 mg/kg) (Escherichia coli, serotype O55:B5) and were ventilated for 6 h. Both endotoxin doses resulted in impaired gas exchange and systemic inflammation in the preterm lambs. Lambs at 141 d GA (term 146 d) were given either 10 mg/kg intratracheal endotoxin, 10 mg/kg endotoxin plus high tidal volume ventilation for the first 30 min of life, or 5 microg/kg endotoxin given intravenously. Endotoxin alone (10 mg/kg) caused lung inflammation but no systemic effects after 6 h of ventilation. Lambs given 10 mg/kg endotoxin plus high tidal volume ventilation or 5 microg/kg endotoxin intravenously had decreased gas exchange and systemic inflammation. Endotoxin was detected in the plasma of lambs at 130 d GA but not at 141 d GA. Inflammation in the lungs was more severe in preterm animals. Mechanical ventilation of the endotoxin-exposed preterm lung resulted in systemic effects at a low endotoxin dose and without high tidal volume ventilation.

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Surfactant Treatment Effects on Lung Structure and Type II Cells of Preterm Ventilated Lambs

Cited by 12 publications

References 31 publications

The Long-term Impacts of Birth Weight and Respiratory Complications after a Preterm Birth

The Long-term Impacts of Birth Weight and Respiratory Complications after a Preterm Birth

Positive End-Expiratory Pressure and Tidal Volume During Initial Ventilation of Preterm Lambs

Intratracheal Endotoxin Causes Systemic Inflammation in Ventilated Preterm Lambs

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