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PubMedDate not supplied

Pulmonary surfactants in pulmonary oedema induced by head injury in mice.

A study has been carried out to examine the role of pulmonary surfactants in pulmonary oedema induced by head injury. Pulmonary oedema was induced by head injury in mice by the method of Mackay (5). There was no change in surface tension as well as total phospholipid concentration of the lung between control and test groups suggesting that there was no involvement of lung surfactant sytem in pulmonary oedema induced by head injury. Since the animals in the test group died within a few minutes, possibly there may not have been sufficient time for alteration of lung surfactant system.

Animals↗
PubMed1978

Studies on the fate of pulmonary surfactant in the lung.

1. Radioactively labelled pulmonary surfactant was prepared in an isolated perfused lung system provided with [14C]hexadecanoate. 2. After intratracheal administration of pulmonary surfactant radioactively labelled components were rapidly distributed into different lung fractions, including macrophages (free cells), but most of the radioactive label was accumulated by the lung tissue. 3. Alveolar macrophages, maintained in a variety of culture media in the presence and absence of mineral particles, incorporated a low percentage (11%) of radioactively labelled components when incubated with the surfactant, although evolution of labelled CO2 (6% of the original total activity) suggested that some breakdown of the components had taken place. 4. In similar cultures little intracellular accumulation or extracellular release of non-esterified fatty acids was demonstrated, indicating minimal catabolism of the high-molecular-weight lipid components of surfactant (particularly phosphatidylcholine). 5. However, experiments in vitro designed to simulate the lysosomal degradation of endocytosed surfactant indicated that the macrophage had enzymes capable of releasing non-esterified fatty acids, particularly hexadecanoate, from the lipoprotein complex. 6. It is argued that lung cells, other than alveolar macrophages, may also have a role in surfactant turnover.

Animals↗
PubMed1979

[Effect of the main components of blood on pulmonary surfactant].

The effect of the main blood constituents on surface activity of substrates containing pulmonary surfactant has been investigated. Mixing of hemolysate, serum, albumin, and fibrinogen with lung extracts and washings, their application in the form of a monolayer or administration into the hypophase of the washing monolayer raised the surface tension (ST) of these substrates. Hemoglobin, serum lipids and cholesterol exerted an opposite action. The contact of all above blood constituents, that elicited varied effects on the ST of the medium containing the surfactant with pulmonary vesicles led to an increase in their stability coefficient determined according to the method of Pattle.

Adsorption↗
PubMed1979

Toxic effects of cadmium on the developing rat lung. I. Altered pulmonary surfactant and the induction of respiratory distress syndrome.

The effects of Cd on the growth of the fetal rat lung and the maturation of the pulmonary surfactant system were studied. Pregnant rats received sc injections of cadmium chloride on d 12-15 of gestation. Animals were sacrificed throughout late gestation. Fetal lungs were assayed for pulmonary surfactant lecithin and spingomyelin. Some animals were allowed to give birth and the neonates were observed for symptoms of respiratory distress. The treatment resulted in high fetal mortality and growth retardation. Lung-body weight ratios were reduced by 20-30% in treated fetuses. Pulmonary spingomyelin content was not affected by the Cd absolute quantity but not in lecithin-lung weight ratio on the last days of gestation. Parturition was delayed almost a full day by the Dd treatment, and birth weights were reduced. Of the treated neonates, 11% developed respiratory distress syndrome. All but one of these individuals died and had lungs with hyaline membranes. Prenatal exposure to Cd can (1) cause lung hypoplasia, (2) affect pulmonary surfactant, and (3) induce respiratory distress syndrome in term pups.

Animals↗
PubMedDate not supplied

Characterization of monolayer cultures of type II alveolar pneumonocytes that produce pulmonary surfactant in vitro.

In lung, type II cells are the site of synthesis of phosphatidylcholine (PC), a major component of pulmonary surfactant. Clonal culture methods permit isolation of an epithelial cell strain (L-2) derived from type II cells of intact rat lung capable of active PC production in vitro. Isotopic labeling of these monolayer cultures show that the choline incorporation pathway is the predominant biosynthetic route for PC production. This same pathway is utilized for PC production in whole lung. Three enzymes of this pathway are readily detected in L-2 cells. Determination of specific enzyme activity in monolayers and whole lung indicate that clonally derived L-2 cells are enriched in choline kinase (10-fold), cholinephosphate cytidyl transferase (10-fold) and cholinephosphotransferase activity (5-fold). Our second approach was to develop an in vitro system in which cellular inter-relationships and cell to cell contacts present in whole lung are maintained. This organotypic system is formed by reaggregation of monodispersed fetal rat lung cells into alveolar-like structures (ALS). The ALS are comprised primarily of type II cells as evidenced by the presence of osmiophilic lamellar bodies in the cells. Biosynthesis of these lamellar bodies occurs de novo and type II cells in the ALS continue to synthesize lamellar bodies. Both systems permit study of a variety of agents of pulmonary surfactant production in vitro.

Cells, Cultured↗
PubMed1977

[Physiopathology and clinical aspects of the alveolar surface active system (pulmonary surfactant)].

Existing knowledge of the pulmonary alveolar surfactant system is summarised in monographic form. Particular attention is directed to its physiopathology, synthesis mechanisms, and pathology in man, as well as to the methods used into its clinical investigation. Stress is laid on the importance of the system in the direct or indirect determination of many cardiac and pneumocardiac diseases. Ways in chich deficiencies on the part of this system can be treated are critically discussed.

Adult↗
PubMed1979

Physicochemical properties of dipalmitoyl phosphatidylcholine after interaction with an apolipoprotein of pulmonary surfactant.

We studied the interaction between an apolipoprotein of pulmonary surfactant and the principal lipid found in this material, dipalmitoyl phosphatidylcholine. The apolipoprotein was extracted from canine surfactant and purified to greater than 90% homogeneity. The apolipoprotein was mixed for 16 h at room temperature with dipalmitoyl phosphatidylcholine dispersed in a buffer containing 0.1 M NaCl and 3mM CaCl2. Unbound lipid, unbound protein, and recombinants of lipid and protein were separated by density gradient centrifugation. 71% of the apolipoprotein was found associated with dipalmitoyl phosphatidylcholine. In comparable experiments using bovine plasma albumin about 13% of the albumin was recovered with the lipid. The physicochemical state of the lipid in the apolipoprotein-lipid complex was modified after binding of the protein. A distinct phase transition at 42 degrees C could no longer be detected, and the rate of adsorption to an air-liquid interface of the apolipoprotein-lipid complex was greater than that of the lipid alone. Surface tension vs. surface area isotherms of the dipalmitoyl phosphatidylcholine-apolipoprotein materials, however, were similar to those exhibited by pure dipalmitoyl phosphatidylcholine. The results suggest a physiological role for this apolipoprotein. It may bind to dipalmitoyl phosphatidylcholine under conditions expected in vivo, and may modify the physical properties of the aggregated dipalmitoyl phosphatidylcholine to form domains of lipid in a liquid-crystalline array. The complex dipalmitoyl phosphatidylcholine and apolipoprotein would have the physical properties necessary for its physiological function, allowing it to absorb to the alveolar interface and reduce its surface tension to less than 10 dynes/cm. Dipalmitoyl phosphatidylcholine, by itself, is in a gel-crystalline array below its phase transition temperature (42 degrees C) and would be incapable of effecting these actions.

Animals↗
PubMed1977

Separation and partial characterization of fractions derived from frog lung homogenates. A possible marker system for amphibian pulmonary surfactant.

The purpose of this study is to determine if inframammalian vertebrate (amphibian) lung contains certain nonspecific esterases that have been identified as enzyme markers for mammalian (rat and mouse) pulmonary surfactant. Density gradient centrifugation procedures were utilized to concentrate any surface-active material in frog lung homogenates. Lipid and protein analyses of one of the derived fractions and of pulmonary lavage fluid were consistent with other techniques indicating that these preparations were surface active. A comparison of the nonspecific esterases in the derived fractions and the pulmonary lavage fluid allowed the identification of a nonspecific esterase that has an electrophoretic mobility comparable to one of the nonspecific esterases already identified as an enzyme marker for mammalian (rat and mouse) pulmonary surfactant. These results indicate that these enzyme markers may be useful in the further investigation of the surfactant systems of other inframammalian vertebrates.

Animals↗
PubMed1979

Pulmonary responses to atmospheric pollutants. II. Effect of petrol vapour inhalation on secretion of pulmonary surfactant.

Inhalation of air contaminated with petrol vapour has been shown to produce reduced surfactant levels in the lungs of rats. Pulmonary surfactant was obtained by endobronchial lavage followed by salt extraction and freeze drying to obtain the dry, hydrophobic product. During 45 days of continuous exposure, the lowest yield of surfactant was obtained after 15 days of treatment. During the following 30 days of treatment, the surfactant yield reached a relatively constant level, approximately half the mean value for control animals. Chromatographic analysis indicated no qualitative alteration in the phospholipid components of surfactant with increasing times of exposure to the irritant. It has been possible to correlate biochemical evidence of toxic lung injury with signs of cellular damage obtained from ultrastructural studies.

Animals↗
PubMed1979

Biochemical modifications of pulmonary surfactant after bromhexine derivate injection.

The authors study the influence of bromhexine metabolite VIII on phospholipid and fatty acid composition comparatively to controls. The subcutaneous injection of NA 872 produces on pulmonary surfactant an increase of 43% of total phospholipids. This change in the distribution of phospholipids is shown by the increase of 53% of phosphatidylcholines. A rise of 61.9--74.4% of palmitic acid appears in the phosphatidylcholines of the pulmonary surfactant. It can be noticed that the specific activity of the phosphatidylcholines rises by 31%.

Animals↗
PubMed1978

Differentiation of the pulmonary surfactant system. Disaturated phosphatidylcholine accumulation in fetal rat lung in vivo and in vitro.

Fetal rat lung was placed in organ culture at 15 days gestation (22 days total gestation period), before biochemical and morphological development of the pulmonary surfactant system. At the fifth day of culture numerous Type II cells containing lamellar bodies were present as determined by electron micrography. Phospholipid accumulation in the cultures increased abruptly beginning at 6 days in culture. The phospholipid which accumulated between the sixth and twelfth culture days was composed of 21--27% disaturated phosphatidylcholines. Both the percent of disaturated phosphatidylcholines in the phospholipid fraction and the qualitative pattern of accumulation as a function of time were similar to observations for fetal rat lung developing in vivo. The data presented provide evidence for development of the pulmonary surfactant system in organ culture in vitro.

Animals↗
PubMed1977

Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust.

1. Pulmonary surfactant was isolated from rats that had been exposed to chrysotile asbestos dust for from 3 days to 15 weeks. 2. Asbestos-treated rats showed a progressive increase in amounts of surfactant. After 15 weeks, treated animals contained 4 times as much as non-treated. 3. No significant change was seen in the total protein or total fatty acid composition of surfactant with exposure. 4. The increase in surfactant phosphatidylcholine normally seen on maturation of rat lung was accelerated by exposure of animals to asbestos. 5. An increase in the activity of phosphorylcholine glyceride transferase in lung homogenates and free cell populations was found. 6. Lysosomal phospholipase A was relatively unaffected by dust exposure. 7. It is suggested that the increase in surfactant amounts could be due to an increase in its synthesis without a corresponding alteration in its degradation.

Animals↗
PubMed1978

Studies of factors influencing lung stability: biochemical changes of pulmonary surfactant and morphological changes of terminal air spaces in the developing rat.

Aging changes of the pulmonary surfactant were studied with regard to phospholipids and cholesterol and to the physical properties in the rat. Newborn rats had remarkably high content of lecithin compared to other age groups and the content was lowest at around 5 days after birth on the basis of wet weight of lungs. Calculated concentration per unit area of alveolar surface based on the body weight was highest in newborn rats and it fell down abruptly at 3 days after birth followed by a gradual decrease to adult level. The content of cholesterol was lowest and the lecithin:cholesterol ratio was highest in the newborn surfactant. The ratio was the same among rats at other ages. Surface activity examined by Wilhelmy balance was not different between newborn and adult with respect to minimum surface tension and stability index but surface spreading of surfactant was faster in neonatal surfactant than in the adult one. The size of the termnal air spaces was remarkably large at birth. It decreased gradually after birth with its minimum at around 17 days after birth and again it increased to adult level. From these observations it was concluded that high stability of excised lungs of normal newborn rats is brought about by these biochemical and morphological differences and these characteristics seem to facilitate the adaptation of lungs to normal breathing at birth.

Aging↗
PubMed1979

Acceleration of pulmonary surfactant maturation in stresses pregnancies: a study of neonatal lung effluent.

To determine the maturation of pulmonary surfactant at birth, phospholipid patterns in tracheal or pharyngeal aspirates of 54 newborn infants were analyzed by two-dimensional thin-layer chromatography. The compositions of phospholipids and their surface tension-lowering abilities were assessed after gestations with various complications. Preterm infants with respiratory distress syndrome (RDS) lacked phosphatidylglycerol and had lower lecithin/sphingomyelin ratios than infants without RDS. An acceleration of both phosphatidylcholine (lecithin) and phosphatidylglycerol concentrations was observed in 21 preterm infants born after prolonged rupture of the membranes and treatment with isoxuprine. In these infants, the phospholipid pattern of lung effluent was similar to that of term infants even at gestational ages less than or equal to 30 weeks. Biochemical lung maturation was delayed in aneccephalic infants, infants of diabetic mothers, and one infant of a mother with hypothyroidism.

Birth Weight↗
PubMed1977

Metabolism of the apoproteins in pulmonary surfactant.

Two proteins having nominal molecular weights of 35,000 and 10,000 daltons are found in pulmonary surfactant. Although experiments on their immunological properties suggest that they share antigenic determinants, their metabolic relationship is unknown. To study this question we injected [14C]palmitic acid or L-[3H]leucine into the femoral vein of 59 puppies. We killed the animals 30 min to 68 h after injection and purified surface-active material from the endobronchial lavage fluid. We isolated the 35,000 apoprotein, the 10,000 apoprotein, and the saturated phosphatidylcholines in surfactant and measured their specific activities at various times after injection. We found that the 35,000 apoprotein appears in alveolar surfactant with the same time course as saturated phosphatidylcholine but is cleared more rapidly than is the lipid. The specific activity of the 10,000 apoprotein reaches a maximum after that seen for the 35,000 apoprotein and decays with the same turnover time as that of the lipid. The kinetic data suggest that the 10,000 apoprotein is a metabolic product of the 35,000 apoprotein. They are not consistent with the possibility that the 10,000 apoprotein is an artifact of nonspecific degradation during preparation.

Amino Acids↗
PubMed1977

Pulmonary surfactant and amniotic fluid insulin.

Immunoreactive insulin was measured in 66 amniotic fluid samples and the level compared to two indices of pulmonary surfactant activity, namely, lecithin sphingomyelin ratio and lecithin palmitic acid. An apparent inverse relation between lecithin and insulin was demonstrated after 34-35 weeks' gestation. These results tend to support the hypothesis that insulin can inhibit lecithin synthesis.

Adult↗