Interaction of Alveolar Surfactant with Plasma-Derived Proteins, Especially Fibrin Monomer, as Causative Principle of Surfactant Dysfunction

Seeger, W.; Stöhr, G.; Wolf, H.; Neuhof, H.

doi:10.1159/000410019

Cited by 3 publications

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“…This phe nomenon is also modified by the phospho lipid composition and concentration, the carrier and the method of preparation; and furthermore the conditions of the lung, such as fluids or proteins in the alveoli, also neu tralize its effect [40,41]. Moreover, the tensioactive effect was not uniform throughout the lung ( fig.…”

Section: Discussionmentioning

confidence: 99%

“…5). Ventilation, greater in the upper lobes, may distribute surfactants ac cording to their liposome weight and spread ing capacity, and the use of a positive end expiratory pressure may help to attain the surface tension equilibrium [24] and favor their distribution producing a more uniform response [36], Variations of alveolar expansion were sig nificantly dependent on body weight, corre lated with lung maturity [41]. To avoid this effect we used the TIAD (alveolar distention excluding the pondéral effect of body weight) obtaining more uniform results.…”

Section: Discussionmentioning

confidence: 99%

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Factors That Influence the Distention of Immature Lung with Artificial Surfactant

Ferrer-Roca

Padilla²,

Doménech³

1990

Neonatology

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The exogenous therapy of respiratory distress syndrome with artificial surfactants is controversial. In the present work we treated premature rabbits with artificial ultrasonic obtained surfactant suspensions [dipalmitoyldiphosphatidylcholine:dipalmitoyldiphosphatidylglycerol (DPPCDPPG) 7:3] in various physical conditions produced by changing the carrier (saline solution and amniotic fluid) or incubating at 41 °C. Nonincubated samples (S0) were nonactive, the best effect on alveolar distention being found after 8 h incubation (S8), while 16 h incubated samples (S16) were less effective. Liposomal size of the mixtures correlated with their effectiveness; small unilamellar liposomes were nonactive, large unilamellar ones were active and in presence of large multilamellar liposomes the tensioactive effect decreased. Fifty-one percent of the alveolar distention, evaluated by morphometry, was due to treatment and 11% was linearly related to body weight. The ponderal effect of body weight was mathematically excluded in order to obtain more uniform results; the resulting parameter was called true treatment influence on alveolar distention (TIAD). 15% of TIAD varied due to the carrier, with significantly better results when saline solution was used as a carrier. These findings question the hypothesis of the prevention of respiratory distress syndrome by means of intraamniotic injection of surfactants.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Factors That Influence the Distention of Immature Lung with Artificial Surfactant

Ferrer-Roca

Padilla²,

Doménech³

1990

Neonatology

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Pulmonary surfactant-associated protein A enhances the surface activity of lipid extract surfactant and reverses inhibition by blood proteins in vitro

Cockshutt¹,

Weitz²,

Possmayer³

1990

Biochemistry

257

161

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Although a monolayer of dipalmitoylphosphatidylcholine, the major component of pulmonary surfactant, is thought to be responsible for the reduction of the surface tension at the air-liquid interface of the alveolus, the participation of unsaturated and anionic phospholipids and the three surfactant-associated proteins is suggested in the generation and maintenance of this surface-active monolayer. We have examined the effects of surfactant-associated protein A (SP-A) purified from bovine lavage material on the surface activity of lipid extract surfactant (LES), an organic extract of pulmonary surfactant containing all of the phospholipids and SP-B and SP-C, but lacking SP-A. Measurements of the surface tension during dynamic compression were made on a pulsating bubble surfactometer. Addition of SP-A to LES reduces the number of pulsations required to attain surface tensions near zero at minimum bubble radius. This increase in surface activity is dependent upon the presence of Ca2+ in the assay mixture. Maximal enhancement is observed at or below 1% of the lipid concentration (w/w). The addition of two blood proteins, fibrinogen and albumin, at physiological concentrations to LES causes severe inhibition of surface activity. Addition of SP-A in the presence of Ca2+ completely counteracts the inhibition by fibrinogen. The amount of SP-A required for full reversal of this inhibition was less than 0.5% of the lipid concentration. Complete reversal of inhibition by albumin was also observed, even though there was a approximately 5000-fold molar excess of inhibitor. Addition of lysophosphatidylcholine also inhibits LES; however, SP-A has no effect on this inhibition.

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Liposome-entrapped antioxidant enzymes prevent lethal O2 toxicity in the newborn rat

Tanswell¹,

Freeman²

1987

Journal of Applied Physiology

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Newborn rat pups delivered and maintained in greater than 95% O2 had a lethal time for 50% of population (LT50) of 13 days. Daily intraperitoneal injection per se did not alter the mortality due to inhalation of O2. Survival after 13.5 days of exposure increased from 40 +/- 7% of pups that received buffered saline only to 95 +/- 4% of pups that received liposomes containing superoxide dismutase and catalase. Daily injection of control liposomes containing no enzymes also caused a less dramatic, though significant, increase in survival from 40 +/- 7 to 71 +/- 7% of O2-exposed pups, indicating that the lipid vehicle, as well as the liposome-entrapped antioxidant enzymes, contributed to the protective effect. The component of the protective effect that could be attributed to the antioxidant enzymes was lost if inactive catalase was used in liposome preparation.

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Interaction of Alveolar Surfactant with Plasma-Derived Proteins, Especially Fibrin Monomer, as Causative Principle of Surfactant Dysfunction

Cited by 3 publications

References 0 publications

Factors That Influence the Distention of Immature Lung with Artificial Surfactant

Factors That Influence the Distention of Immature Lung with Artificial Surfactant

Pulmonary surfactant-associated protein A enhances the surface activity of lipid extract surfactant and reverses inhibition by blood proteins in vitro

Liposome-entrapped antioxidant enzymes prevent lethal O2 toxicity in the newborn rat

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