Surface active materials from dog lung. II. Composition and physiological correlations

King, R. E.; Clements, J. A.

doi:10.1152/ajplegacy.1972.223.3.715

Cited by 512 publications

(160 citation statements)

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“…Therefore, infants may be dependent on nutritional sources of carnitine, such as milk. Infants receiving carnitine-free total parenteral nutrition are at risk of developing carnitine deficiency characterized by decreased blood concentration and tissue content of carnitine (2, 20,24,28). Reduced carnitine intake may impair fatty acid oxidation and diminish ketogenesis after fat infusion; these deficiencies can be corrected with supplementary carnitine (23,29).…”

Section: Discussionmentioning

confidence: 99%

Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

1985

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ABSTRAm. The possibility that pulmonary surfactant, characterized by a phosphatidylglycerol deficiency, as in early fetal life, might have inferior surface properties was evaluated. We obtained this specific surfactant from adult rabbits by withholding glucose and giving them an excess of myoinositol by mouth and intravenously. Controls were given a similar quantity of glucose. The myoinositol resulted in a drastic reduction of surfactant phosphatidylglycerol, from 7.2 to 0.3% of phospholipids, and a corresponding increase in phosphatidylinositol from 4.8 to 11.3%. In addition, the myoinositol treatment increased the myoinosit01 that was disaturated from 18.5 to 27.3% ( p < 0.05).

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Section: Discussionmentioning

confidence: 99%

Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

1985

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“…The mucociliary transport rate was expressed as an average of the total measure ment during a 10 min period after ACh nebulizing (control) and during a 10 min period after acid-nebulizing, respectively. The composition of surface active phospholipids shown in Table 1 was based on the concen trations of those in pulmonary surfactant (11,12 2. Effect of ACh on mucociliary transport: Nebulizing ACh caused an approximately 70% increase in the mucociliary transport rate, and the increase lasted for 50 min (Fig.…”

Section: Methodsmentioning

confidence: 99%

Protective effect of surface-active phospholipids against the acid-inducing inhibition of the tracheal mucociliary transport.

Kai¹,

Saito²,

Furusawa³

et al. 1989

Jpn.J.Pharmacol

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Abstract-Littleis known about the physiological role of surface active phos pholipids (SAP) in the central respiratory tract.In the present study, the effect of SAP on acid-inducing inhibition of particle transport by the tracheal mucociliary function was investigated in unanesthetized pigeons. SAP and acids were directly nebulized to the surface of the trachea.The composition of SAP was based on that of the pulmonary surfactant.The experiment was carried out under application of acetylcholine providing a constant mucociliary transport. SAP significantly diminished HCI and H2S04-inducing inhibitions of the mucociliary transport. Benzalkonium chloride also reduced the inhibition.The results suggest that SAP may be a protecting factor of the mucociliary clearance and that SAP may be con nected with hydrophobicity not only of the alveolar surface but of the tracheal epithelium.

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“…SP-A and SP-D may play important roles in the first line defense against inhaled pathogens, and SP-A may have a regulatory function in the formation of the monolayer that lowers the surface tension. In 1972 King and Clements reported that canine surfactant lipids were able to form stable surface films with low surface tension but that this process was much faster when complete canine surfactant with the proteins included was used [170]. This important observation indicated that the presence of the surfactant-associated proteins was required for an optimal functioning of the lung.…”

Section: Composition 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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Surface active materials from dog lung. II. Composition and physiological correlations

Cited by 512 publications

References 0 publications

Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

Protective effect of surface-active phospholipids against the acid-inducing inhibition of the tracheal mucociliary transport.

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

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