Effects on Experimental Acute Lung Injury 24 Hours After Exogenous Surfactant Instillation

Anderson, Blair M.; Jackson, F; Moxley, Michael A.; Longmore, William J.

doi:10.3109/01902149209031680

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…Comparison of air-and fluid-filled pressure volume profiles in isolated lungs of animals with experimental ARDS indicates that increases in static elastic recoil after acute inflammation are due to abnormalities in surfactant function and not to changes in tissue elastic recoil (13). An in vivo animal study (1) has demonstrated surfactant dysfunction after capillary leakage due to chemical injury. To date, the biochemical and biophysical processes that relate inflammation to alterations in surfactant function are not well understood.…”

mentioning

confidence: 99%

Determinants of surfactant function in acute lung injury and early recovery

Mora

Arold

Marzan

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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Relationships between lung function and surfactant function and composition were examined during the evolution of acute lung injury in guinea pigs. Lung mechanics and gas exchange were assessed 12, 24, or 48 h after exposure to nebulized lipopolysaccharide (LPS). Bronchoalveolar lavage (BAL) fluid was processed for phospholipid and protein contents and surfactant protein (SP) A and SP-B levels; surfactant function was measured by pulsating bubble surfactometry. Lung elastance, tissue resistance, and arterial-alveolar gradient were moderately elevated by 12 h after LPS exposure and continued to increase over the first 24 h but began to recover between 24 and 48 h. Similarly, the absolute amount of 30,000 g pelleted SP-A and SP-B, the phospholipid content of BAL fluid, and surfactant function declined over the first 24 h after exposure, with recovery between 24 and 48 h. BAL fluid total protein content increased steadily over the first 48 h after LPS nebulization. In this model of acute lung injury, the intra-alveolar repletion of surfactant components in early recovery led to improved surfactant function despite the presence of potentially inhibitory plasma proteins.

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mentioning

confidence: 99%

Determinants of surfactant function in acute lung injury and early recovery

Mora

Arold

Marzan

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Many animal and clinical studies have demonstrated positive effects of either ESS alone or PLV alone on ALI induced by causes other than smoke inhalation (17)(18)(19)(20)(21)(22)(23)(24). Additionally, several studies with newborn or premature animals have shown the beneficial effects of a combined therapy of ESS and PLV on ALI induced by repeated saline lavage (25)(26)(27)(28)(29).…”

mentioning

confidence: 99%

Effects of exogenous surfactant supplementation and partial liquid ventilation on acute lung injury induced by wood smoke inhalation in newborn piglets

Jeng

Kou

Sheu

et al. 2003

Critical Care Medicine

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“…A second disease for which administration of synthetic surfactant could be useful is ARDS [8,95]. (For a review, see Ref.…”

Section: Therapeutic Use Of Surfactantmentioning

confidence: 99%

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

283

188

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Abstract. This article starts with a brief account of the history of research on pulmonary surfactant. We will then discuss the morphological aspects and composition of the pulmonary surfactant system. We describe the hydrophilic surfactant proteins A and D and the hydrophobic surfactant proteins B and C, with focus on the crucial roles of these proteins in the dynamics, metabolism, and functions of pulmonary surfactant. Next we discuss the major disorders of the surfactant system. The final part of the review will be focused on the potentials and complications of surfactant therapy in the treatment of some of these disorders. It is our belief that increased knowledge of the surfactant system and its functions will lead to a more optimal composition of the exogenous surfactants and, perhaps, widen their applicability to treatment of surfactant disorders other than neonatal respiratory distress syndrome.Key words: Surfactant protein-Pulmonary surfactant-Respiratory distress syndrome. HistoryResearch on surfactant goes back to 1929 when von Neergaard published the first paper about the difference in pressure needed to inflate lungs with air or with liquid [333]. He found that the pressure necessary for filling the lungs with air was higher than when the lungs were filled with liquid. To explain this result he stated that the alveoli were stabilized by lowering the naturally high surface tension of the air/water interface. In 1946 Thannhauser and co-workers reported that lung tissue has a remarkably high content of the lipid dipalmityl lecithin (current name, dipalmitoylphosphatidylcholine)Offprint requests to: Henk P. Haagsman.

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Effects on Experimental Acute Lung Injury 24 Hours After Exogenous Surfactant Instillation

Cited by 11 publications

References 24 publications

Determinants of surfactant function in acute lung injury and early recovery

Determinants of surfactant function in acute lung injury and early recovery

Effects of exogenous surfactant supplementation and partial liquid ventilation on acute lung injury induced by wood smoke inhalation in newborn piglets

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

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