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PubMed2000

Preservation of intraalveolar surfactant in a rat lung ischaemia/reperfusion injury model.

Ischaemia/reperfusion (I/R) injury, a major problem in clinical lung transplantation, is associated with surfactant dysfunction. The present study aimed to test the hypothesis that preservation related improvements in post-ischaemic lung function are associated with improved ultrastructural preservation of pulmonary surfactant. Rat lungs were flush perfused with modified Euro-Collins solutions (ECS), stored for 2 h at 4 degrees C, and reperfused for 40 min. Lungs were preserved with conventional (ECS 115: 115 mmol x L(-1) K+), medium-K+ (ECS 40: 40 mmol x L(-1) K+), or low-K+ (ECS 10: 10 mmol x L(-1) K+) ECS. Functional parameters were monitored during reperfusion (n=10 per group). After reperfusion, left lungs were prepared for electron microscopical and stereological analysis of surfactant (n=5 per group). In all three experimental groups notable I/R injury developed which was lowest in ECS 40 as indicated by significantly less intraalveolar oedema, higher perfusate oxygenation, and lower peak inspiratory pressure. This was associated with a significantly superior preservation of the ultrastructure of the surface active surfactant subtype tubular myelin in ECS 40 compared with ECS 115 and ECS 10. Stereological analysis revealed that the relative amount of tubular myelin was highest in ECS 40 (mean+/-SEM; 6.2+/-0.8%) compared with ECS 115 (3.0+/-1.0%) and ECS 10 (2.7+/-1.6%). Analysis of surfactant in its natural location within the organ showed that the severity of ischaemia/reperfusion injury correlates with differences in intraalveolar surfactant composition. Improved post-ischaemic respiratory function achieved by medium-K+ Euro-Collins solution is associated with superior ultrastructural preservation of tubular myelin. It is concluded that the integrity of surface active tubular myelin represents an important criterion for the assessment of lung preservation quality.

Animals↗

PubMed1996

Use of surfactant in pulmonary disorders in full-term infants.

Pulmonary surfactant is routinely used for treatment of premature babies with respiratory distress syndrome, and its use in full-term infants with respiratory failure is now under extensive clinical investigation. Several clinical reports have shown that intratracheal instillation of large doses of bovine and porcine lung-derived surfactant preparations has the potential to improve blood oxygenation and ventilation efficiency in full-term neonates with respiratory distress syndrome, meconium aspiration syndrome, pneumonia, pulmonary hemorrhage, and lung hypoplasia. These findings are suggestive of secondary surfactant deficiency or surfactant dysfunction in the pathogenesis of respiratory failure in full-term infants. Further clinical investigation with multicenter, randomized, controlled clinical trials is warranted to verify new indications of surfactant application for these diseases.

Extracorporeal Membrane Oxygenation↗

PubMed2005

Inhibition of surfactant activity by Pneumocystis carinii organisms and components in vitro.

This study examines the direct inhibitory effects of Pneumocystis carinii (Pc) organisms and chemical components on the surface activity and composition of whole calf lung surfactant (WLS) and calf lung surfactant extract (CLSE) in vitro. Incubation of WLS suspensions with intact Pc organisms (10(7) per milligram of surfactant phospholipid) did not significantly alter total phospholipid levels or surfactant protein A content. Incubation with intact Pc organisms also did not impair dynamic surface tension lowering in suspensions of WLS or centrifuged large surfactant aggregates on a bubble surfactometer (37 degrees C, 20 cycles/min, 0.5 and 2.5 mg phospholipid/ml). However, exposure of WLS or CLSE to disrupted (sonicated) Pc organisms led to severe detriments in activity, with minimum surface tensions of 17-19 mN/m vs. <1 mN/m for surfactants alone. Extracted hydrophobic chemical components from Pc (98.8% lipids, 0.1 mM) reduced the surface activity of WLS and CLSE similarly to sonicated Pc organisms, whereas extracted hydrophilic chemical components from Pc (primarily proteins) had only minor effects on surface tension lowering. These results indicate that in addition to surfactant dysfunction induced by inflammatory lung injury and edema-derived inhibitors in Pc pneumonia, disrupted Pc organisms in the alveolar lumen also have the potential to directly inhibit endogenous and exogenous lung surfactants in affected patients.

Animals↗

PubMed1996

In vitro effect of meconium on the physical surface properties and morphology of exogenous pulmonary surfactant.

The pathophysiology of meconium aspiration syndrome(MAS) is related to mechanical obstruction of the airways and to chemical pneumonitis. Meconium is also suggested to cause functional deterioration of pulmonary surfactant. Recent studies have reported that meconium inhibits the physical surface properties of pulmonary surfactant, and that administration of exogenous surfactant may provide therapeutic benefits in animal models or infants with respiratory distress due to MAS. To assess the effects of meconium on physical surface properties, especially the changes on the air-liquid interface and hypophase of pulmonary surfactant in vitro, we studied the following findings; a) the surface spreading rate(SSR) and the surface adsorption rate(SAR), b) the viscosity, c) the electron microscopic changes, on a series of mixtures with various concentrations of lyophilized human meconium and Surfactant-TA(SurfactenTM). The human meconium has significantly increased the surface tension of SSR and the viscosity of pulmonary surfactant, but had decreased the surface pressure of SAR of surfactant, and changed the electron microscopic findings of surfactant. We have concluded that these findings support the concept that meconium-induced surfactant dysfunction may play a role in the pathophysiology of MAS.

Humans↗

PubMed2000

Influence of modified natural or synthetic surfactant preparations on growth of bacteria causing infections in the neonatal period.

Connatal bacterial pneumonia is common in neonates. Animal studies and initial clinical reports indicate that surfactant dysfunction is involved in the pathophysiology of severe neonatal pneumonia. Since respiratory distress syndrome and connatal pneumonia may be difficult to differentiate in the first hours of life, neonates with respiratory failure due to bacterial infections might receive surfactant. Under such conditions surfactant components might be catabolized by bacteria and promote bacterial growth. We therefore investigated the influence of three modified natural (Curosurf, Alveofact, and Survanta) and two synthetic (Exosurf and Pumactant) surfactant preparations on the growth of bacteria frequently cultured from blood or tracheal aspirate fluid in the first days of life. Group B streptococci (GBS), Staphyloccocus aureus, and Escherichia coli were incubated in a nutrient-free medium (normal saline) for 5 h at 37 degrees C, together with different surfactants at concentrations of 0, 1, 10, and 20 mg/ml. With the exception of E. coli, incubation in saline alone led to a variable decrease in CFU. In the presence of Alveofact, Exosurf, and Pumactant the decline in bacterial numbers was less marked than in saline alone. Curosurf was bactericidal in a dose-dependent fashion for GBS and had a strong negative impact on the growth of a GBS subtype that lacked the polysaccharide capsule. In contrast, Survanta (10 and 20 mg/ml) significantly promoted the growth of E. coli, indicating that surfactant components may actually serve as nutrients. We conclude that bacterial growth in different surfactant preparations is influenced by microbial species and the composition and dose of the surfactant. Further studies are necessary to elucidate the mechanisms behind our findings and to evaluate the effects of surfactant on bacterial growth in vivo.

Biological Products↗

PubMed2000

Surfactant protein SP-B counteracts inhibition of pulmonary surfactant by serum proteins.

In addition to the primary surfactant deficiency in newborns with respiratory distress syndrome (RDS), in the later course of RDS substantial protein leakage into the alveolar spaces can occur by damage to the alveolocapillary membrane. Acute lung injury results in surfactant dysfunction due in part to inhibition by serum proteins. The aim of this study was to investigate the influence of SP-B on the inhibitory effects of albumin (alb) and fibrinogen (fib) on the surface activity of pulmonary surfactant, using a) surface tension measurement with the pulsating bubble surfactometer in suspensions and b) in surfactant films applying the hypophase exchanger. After hypophase exchange a preformed film of Survanta is very resistant to the inhibitory activity of alb or fib. The surface tensions of suspensions are significantly higher (p <0.001) than the surface tensions of preformed surfactant films if alb or fib were added, e.g., 42 (41 to 43) mN/m vs. 21 (19 to 22) mN/m for Survanta with 20 mg alb/ml. After additional supplementation of Survanta with SP-B the surface activity of Survanta/1% SP-B films did not show inhibition by fib (2 mg/ml), (surface tension 8 (4 to 13) mN/m). These results indicate that SP-B can play an important role to protect the pulmonary surfactant film from inactivation by serum proteins.

Fibrinogen↗

PubMed2003

[Influence of inhaled nitric oxide on surfactant in the total cardiopulmonary bypass pig model].

OBJECTIVE: To study whether or not inhaled nitric oxide (INO) can improve surfactant production and pulmonary mechanics after CPB in pigs, and to seek the mechanism of lung injury during mechanical ventilation. METHODS: Thirty pigs were randomized into 6 groups: Sham (n = 5), Sham + INO (n = 5), CPB (n = 5), CPB + INO (n = 5), CPB + lipopolysaccharide (LPS) (n = 5), and CPB + LPS + INO (n = 5). After anesthesia induction, INO (mass fraction, 20 x 10(-6)), added to the gas mixture, was given to the animals throughout the procedure. After 2 hours of INO treatment, broncho-alveolar lavage (BAL) fluid was taken for surfactant assay and cytology analysis. Pulmonary hemodynamics parameters and lung compliance were measured as well. CPB was performed for 90 minutes after the first BAL sampling at T0. Four hours (T4) and 24 hours (T24) following CPB, BAL and other measurements were repeated. After CPB, LPS (4 micrograms.kg-1) was infused to specific groups of pigs within 90 minutes in order to stimulate the inflammation process. RESULTS: Pulmonary hemodynamics parameters (pulmonary artery pressure, pulmonary vascular resistance and oxygenation) in all INO groups were much better than those of the control groups at T4 and T24. However, lung compliance of pigs in all groups declined with time, and showed statistically significant differences at T24 compared with T0. At T0, the active subfraction of surfactant (large aggregate, LA) was increased in animals given INO treatment compared with the controls, but decreased with time, and at T24 significantly reduced in all groups. In LPS groups, this decrease LA after T4 was very obvious. Total cell counts and the percent differentials of neutrophils in BAL increased with time, being lower in the INO groups than in other groups. CONCLUSION: INO exposure exerted time-related effects on the lung surfactant (LA). Initially, INO resulted in short-term increase of surfactant production at T0. However, with time passing by, INO exposure following CPB did not prevent long-term decrease of lung surfactant and lung compliance although INO was beneficial for pulmonary hemodynamics and oxygenation. In summary, despite the use of INO, synergetic effects of long-term hyperoxia, mechanical ventilation and inflammation following CPB may exacerbate pulmonary mechanics and result in surfactant dysfunction.

Administration, Inhalation↗

PubMed1992

Integrity of the alveolar-capillary barrier and alveolar surfactant system in smokers.

BACKGROUND: The permeability of the alveolar-capillary barrier to technetium-99m labelled diethylenetriamine pentaacetate (99mTc DTPA) is known to be greatly increased in smokers, but the underlying mechanism is poorly understood. Abnormal permeability of the alveolar epithelium as well as impaired surfactant function has been suggested. The purpose of this study was to examine transudation of urea and albumin into the alveoli and alveolar surfactant function in smokers and non-smokers and to relate these variables to the rate of alveolar-capillary transfer of 99mTc DTPA. METHODS: Standardised bronchoalveolar lavage was performed and the yield of urea and albumin measured in the lavage fluid. The integrity of the alveolar surfactant system was assessed by measurement of the surface activity and of the yield of phospholipids in alveolar lavage fluid. RESULTS: The mean decay constant for the pulmonary clearance of 99mTc DTPA was 0.028/min in the smokers and 0.009/min in the non-smokers. The recovery of albumin and urea in alveolar lavage fluid was very similar in the two groups. The surface activity of alveolar lavage fluid was lower in smokers than in non-smokers (minimum surface tension 37.9 versus 28.6 mN/m) and the yield of phospholipids was reduced (2.08 versus 3.86 mg). The rate constant for the pulmonary clearance of 99mTc DTPA correlated with the yield of phospholipids at bronchoalveolar lavage. CONCLUSIONS: The study shows that increased alveolar-capillary transfer of 99mTc DTPA in smokers is not accompanied by increased transudation of small or large molecules into the alveoli. The findings support the hypothesis that increased clearance of 99mTc DTPA in smokers is related to surfactant dysfunction.

Adult↗

PubMed1993

Disruption of pulmonary surfactant's ability to maintain openness of a narrow tube.

Pulmonary surfactant stabilizes alveoli but, by maintaining patency of peripheral conducting airways, will also lower resistance to airflow. A small quantity of a surfactant suspension (3 mg/ml) formed a blocking liquid column in a narrow section of a glass capillary. Pressure was raised on one side of that column, whereby it was forced to move out of the narrow section, and it did not return but left the capillary open for a free airflow. The surfactant capability to maintain free airflow was lost with the addition of albumin (> 10 mg/ml) or fibrinogen (> 0.5 mg/ml). Surfactant function was seriously affected by hydrolysis with phospholipase C but not with phospholipase A2. With a small quantity of albumin added (5 mg/ml), the ability to maintain openness was seriously affected at temperatures below 25 degrees C. An inflammatory reaction due to atopy, infection, or inhalation of irritating gases characterizes a variety of airway diseases, including asthma. If the in vitro studies can be transferred to in vivo conditions, surfactant dysfunction might contribute to certain types of airway disease.

Animals↗

PubMed1986

A protein that inhibits surfactant in respiratory distress syndrome.

A protein that interferes with surfactant function is present in the airways and alveoli of infants with respiratory distress syndrome (RDS). This inhibitor is also found in serum and amniotic fluid and presumably appears in the alveoli because of the abnormal protein leak present in the lungs of infants with RDS. This protein has a molecular weight of about 110,000 and is resistant to boiling or lipid extraction. As measured by radioimmunoassay, the ratio of inhibitor to phosphatidylcholine decreased from 8.1 +/- 2.3 early in the course of RDS to 0.7 +/- 0.1 on the day of extubation. The value at extubation was the same as that measured for preterm infants without RDS. The inhibitor to phosphatidylcholine ratio in airway samples from infants with RDS correlated significantly with simultaneously recorded pO2/FiO2 ratios and the peak inspiratory pressures used to normalized pCO2 values. These results are consistent with the concept that the inhibitor contributes to surfactant dysfunction and thus the respiratory failure characteristic of RDS.

Amniotic Fluid↗

PubMed1988

Sublethal hyperoxic injury to the alveolar epithelium and the pulmonary surfactant system.

We quantified the effects of continuous exposure to 100% O2 on the development of sublethal injury to the pulmonary alveolar epithelium of rabbits. There was a progressive increase in alveolar permeability to solute after 48 h in O2, which coincided with the onset of damage to the pulmonary microvasculature. Rabbits that were exposed to 100% O2 for 64 h and returned to room air for 24 h had, in addition to increased permeability to solute, decreased phospholipid levels, decreased total lung capacity, pulmonary edema, high minimum surface tensions in their bronchoalveolar lavage, and moderate hypoxemia. Intratracheal instillation of calf lung surfactant (CLSE) significantly ameliorated the progression of hyperoxic injury by increasing alveolar phospholipid levels and thus preventing the inhibition of lung surfactant activity by plasma proteins and other high molecular weight components of alveolar edema. We concluded that the alveolar epithelium and the pulmonary microvasculature show similar sensitivity to hyperoxia and that clinical manifestations of hyperoxic lung injury may be due, at least in part, to surfactant dysfunction.

Animals↗

PubMed2000

Lung function, permeability, and surfactant composition in oleic acid-induced acute lung injury in rats.

Although acute lung injury (ALI) is associated with inflammation and surfactant dysfunction, the precise sequence of these changes remains poorly described. We used oleic acid to study the pathogenesis of ALI in spontaneously breathing anesthetized rats. We found that lung pathology can occur far more rapidly than previously appreciated. Lung neutrophils were increased approximately threefold within 5 min, and surfactant composition was dramatically altered within 15 min. Alveolar cholesterol increased by approximately 200%, and even though disaturated phospholipids increased by approximately 30% over 4 h, the disaturated phospholipid-to-total phospholipid ratio fell. Although the alveolocapillary barrier was profoundly disrupted after just 15 min, with marked elevations in lung fluid ((99m)Tc-labeled diethylenetriamine pentaacetic acid) and (125)I-labeled albumin flux, the lung rapidly began to regain its sieving properties. Despite the restoration in lung permeability, the animals remained hypoxic even though minute ventilation was increased approximately twofold and static compliance progressively deteriorated. This study highlights that ALI can set in motion a sequence of events continuing the respiratory failure irrespective of the alveolar surfactant pool size and the status of the alveolocapillary barrier.

Albumins↗

PubMed1996

Effects of human polymorphonuclear leukocyte elastase upon surfactant proteins in vitro.

Recent evidence has suggested that elastase is released by polymorphonuclear leukocytes (PMN) recruited from the pulmonary microcirculation into the alveoli during acute lung injury. This study was undertaken to test the hypothesis that elastase from PMN (PMN elastase) damages or degrades one or more of the surfactant proteins (SP-A, SP-B and SP-C) of the lung, and thereby alters its function. We attempted to use amounts of PMN elastase and quantities of surfactant that would be plausible in the lungs of patients with ARDS. Surfactant from normal dog lungs (2 mg phospholipid, 200 micrograms protein), and purified SP-A (20 micrograms), SP-B (10 micrograms) and SP-C (10 micrograms) from the surfactant (identified by SDS-PAGE and N-terminal amino acid sequences) were incubated for 4-8 h at 37 degrees C with various amounts (0.25-1.0 U) of human PMN elastase purified by affinity chromatography. SDS-PAGE and amino acid composition analysis of the surfactant as well as of the purified SP-A, SP-B, and SP-C showed that degradation of these proteins progressed with incubation time and with the amount of PMN elastase, and was accompanied by decreases in isopycnic density (g/cm3) and surface adsorption, and increase of surface tension of the surfactant. No effects were observed with heat inactivated PMN elastase (95 degrees C, 30 min) or with PMN elastase in the presence of human alpha-1 protease inhibitor (2 micrograms/microgram elastase). Phospholipid compositions of the surfactant after exposure to PMN elastase were not significantly different from those of the controls, suggesting that SP-A, SP-B, and SP-C play a major role in altering the surfactant properties. SP-A was also degraded by elastase and trypsin from pancreas whereas SP-B and SP-C remained intact, providing a natural surfactant without SP-A. Surface adsorption rate of the SP-A deficient surfactant was lower than that of the control, but was much higher than that of the surfactant with completely degraded SP-A, SP-B, and SP-C, suggesting that hydrophobic SP-B and SP-C are the essential components in enhancing adsorption. We conclude that proteolytic degradation of SP-A, SP-B, and SP-C causes the decrease of surfactant isopycnic density, and is responsible for retarding adsorption resulting in surfactant dysfunction.

Amino Acid Sequence↗

PubMed1997

Pulmonary surfactant in cystic fibrosis.

Cystic fibrosis (CF) leads to a chronic inflammation of the airways with significant air flow limitations developing early in the course of the disease. As a well-functioning pulmonary surfactant is necessary to keep the alveoli and the small conducting airways open during expiration, we hypothesized that the biochemical and biophysical properties of surfactant may be impaired in CF. Bronchoalveolar lavage fluid obtained during a clinically stable period was analysed from 20 CF patients (5.9-20 yrs) and 17 healthy children and adults. CF patients had significantly elevated total and polymorphonuclear neutrophil cell counts, whereas the concentrations of total protein and phospholipids did not differ from controls. The percentage of surface active phospholipids, phosphatidylcholine and phosphatidylglycerol, and the concentration of surfactant protein A were significantly reduced in CF patients. Surfactant protein B was unchanged. Although the relative proportion of large aggregates was higher in CF, their surface active properties were inferior, as assessed in the pulsating bubble surfactometer. Because the capacity of CF lavage fractions to inhibit surfactant function was the same as that of controls, impaired minimal surface tension was more likely to be due to the biochemical alterations detected, than to inhibition of a well-functioning surfactant. The impaired pulmonary surfactant system in clinically stable patients with cystic fibrosis is in agreement with the view that surfactant dysfunction may contribute to lung disease in cystic fibrosis.

Adolescent↗

PubMed2000

Overcoming surfactant inhibition with polymers.

Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextran and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration.

Humans↗

PubMed2005

Surface properties of sulfur- and ether-linked phosphonolipids with and without purified hydrophobic lung surfactant proteins.

Two novel C16:0 sulfur-linked phosphonolipids (S-lipid and SO(2)-lipid) and two ether-linked phosphonolipids (C16:0 DEPN-8 and C16:1 UnDEPN-8) were studied for surface behavior alone and in mixtures with purified bovine lung surfactant proteins (SP)-B and/or SP-C. Synthetic C16:0 phosphonolipids all had improved adsorption and film respreading compared to dipalmitoyl phosphatidylcholine, and SO(2)-lipid and DEPN-8 reached maximum surface pressures of 72mN/m (minimum surface tensions of <1mN/m) in compressed films on the Wilhelmy balance (23 degrees C). Dispersions of DEPN-8 (0.5mg/ml) and SO(2)-lipid (2.5mg/ml) also reached minimum surface tensions of <1mN/m on a pulsating bubble surfactometer (37 degrees C, 20cycles/min, 50% area compression). Synthetic lung surfactants containing DEPN-8 or SO(2)-lipid+0.75% SP-B+0.75% SP-C had dynamic surface activity on the bubble equal to that of calf lung surfactant extract (CLSE). Surfactants containing DEPN-8 or SO(2)-lipid plus 1.5% SP-B also had very high surface activity, but less than when both apoproteins were present together. Adding 10wt.% of UnDEPN-8 to synthetic lung surfactants did not improve dynamic surface activity. Surfactants containing DEPN-8 or SO(2)-lipid plus 0.75% SP-B/0.75% SP-C were chemically and biophysically resistant to phospholipase A(2) (PLA(2)), while CLSE was severely inhibited by PLA(2). The high activity and inhibition resistance of synthetic surfactants containing DEPN-8 or SO(2)-lipid plus SP-B/SP-C are promising for future applications in treating surfactant dysfunction in inflammatory lung injury.

Adsorption↗

PubMed1998

Ozone affects breathing and pulmonary surfactant function in mice.

The effect on breathing of BALB/c mice immediately following ozone exposure (2 ppm) for 0, 2, 4, 6, and 8 h was studied with a whole body plethysmograph. Whether such exposure affected the normal function of pulmonary surfactant of maintaining airway patency was evaluated with a capillary surfactometer. Respiratory rate in mice that were not exposed was 358+/-16 (mean+/-S.E.) breaths/min and decreased to 202+/-10 after 6 h exposure. The mean pressure change caused by breathing diminished significantly, indicating a reduced tidal volume. BAL fluid from controls maintained patency for 88+/-2% of the study time, 120 s, implying a good surfactant function, but the ozone exposure caused the surfactant to lose its capability of maintaining patency (P < 0.0001). This decaying surfactant function of the BAL fluid coincided with an increasing protein concentration in the fluid of exposed animals (1.46+/-0.14 mg/ml in the 8-h group) as compared to controls (0.44+/-0.04 mg/ml, P < 0.0001). It is concluded that leakage of plasma proteins into the airway lumen was probably the main reason for the surfactant dysfunction, which may have contributed to the altered breathing pattern.

Animals↗

PubMed1999

Surfactant treatment in a pediatric burn patient with respiratory failure.

This report describes surfactant treatment in a burned infant with severe respiratory failure. In this patient the instillation of surfactant rapidly improved compliance, oxygen index (OI), and alveolar-capillary oxygen gradient (AaDO2), while the need for oxygen supplementation and peak positive pressure drastically decreased. The treatment was repeated after 12 hours. Although the baby had severe clinical course complications as a Gram-negative sepsis and a subglottic stenosis, she was weaned from oxygen therapy and mechanical ventilation in few weeks. Surfactant dysfunctions seem to play a central role in the respiratory insufficiency of burned patients, and its exogenous replacements could improve their outcome.

Burns, Inhalation↗