Lung Surfactant Phospholipids Research Articles

Biophysical activity of synthetic phospholipids combined with purified lung surfactant 6000 Dalton apoprotein

This research studies the biophysical surface activity of synthetic phospholipids combined in vitro with purified lung surfactant apoprotein, having an M r of 6000. Hydrophobic surfactant-associated protein (SAP-6) was delipidated and purified from both bovine and canine lung lavage, and was combined in vitro with a synthetic phospholipid mixture (SM) of similar composition to natural lung surfactant phospholipids. SM phospholipids were also combined and studied biophysically with another purified surfactant-associated protein, SAP-35. The biophysical activity of synthetic phospholipid-apoprotein combinants was assessed by measurements of adsorption facility and dynamic surface tension lowering ability at 37°C. The SM-SAP-6 combinants had adsorption facility equivalent to natural lung surfactant, and to the surfactant extract preparations CLSE and surfactant-TA used in exogenous surfactant replacement therapy for the neonatal Respiratory Distress Syndrome (RDS). The synthetic phospholipid-SAP-6 combinants also lowered surface tension to < 1 dyne/cm under dynamic compression in an oscillating bubble apparatus at concentrations as low as 0.5 mg phospholipid/ml. A striking finding was that this excellent dynamic surface activity was preserved as SAP-6 composition was reduced to values as low as 5 μ/5 mg SM phospholipid (0.1% SAP-6 protein), an order of magnitude less than the 1% protein content of CLSE and surfactant-TA. Mixtures of SM phospholipids plus SAP-35, the major surfactant glycoprotein, had significantly lower biophysical activity, which did not approach that of a functional lung surfactant. These results suggest that synthetic exogenous surfactants of potential utility for replacement therapy in RDS can be formulated by combining synthetic phospholipids in vitro with specifically purified, hydrophobic surfactant-associated protein, SAP-6.

Degradation of dipalmitoyl phosphatidylcholine by isolated rat granular pneumocytes and reutilization for surfactant synthesis.

We investigated metabolic utilization of exogenous (modelled after lung surfactant) phospholipids by granular pneumocytes in primary culture. Cells were incubated for 21, 65, and 140 min with [3H-methyl]dipalmitoylphosphatidylcholine (DPPC) containing liposomes prepared from synthetic lipids. Radioactivity in cellular phosphatidylcholine (PC) declined steadily to 50% of the total trypsin-resistant cell-associated radioactivity. The proportion of radioactivity increased with time in cytidine-5'-diphosphate-choline and phosphorylcholine, which suggested reutilization of choline for PC synthesis. Cells incubated with liposomes for 2 h revealed that of the total cell-associated radioactivity, 7% was in lamellar bodies and 10% in the microsomal fraction. The lipid-associated radioactivity was 24% in "soluble," 96% in lamellar bodies, and 92% in the microsomal fraction. Percent of total PC label recovered in disaturated PC of microsomal fractions decreased (slope = -5.27%/h) with time of incubation (r = 0.67). Incubation of cells with liposomes containing ([3H-methyl]choline-[14C]palmitoyl) DPPC led to altered isotope ratios in both lamellar bodies and microsomes. These observations indicate that granular pneumocytes degrade exogenous PC and resynthesize PC from degradation products.

UPTAKE OF THE MAJOR SURFACTANT APOPROTEIN BY NEONATAL LUNG TISSUE

Secreted lung surfactant phospholipid has been shown to be recycled by alveolar type II cells. We hypothesize that the 35 kDa surfactant apoprotein (SAP) participates in surfactant reutilization. SAP was purified from rabbit lung lavage, radiolabeled with [125I], and instilled, along with carrier surfactant, into the lungs of neonatal rabbits. After intervals of 0, 5, 15, 30 or 60 minutes, the rabbits were sacrificed, their lungs lavaged, then the lung tissue homogenized. Uptake of [125I]-SAP by the lung tissue was significant and time-dependent, reaching 16.9 ± 1.6% of the amount originally instilled by 1 hour. Less than 1% of the instilled [125I]SAP was detected in blood, liver and kidney. These data are suggestive that instilled [125I]SAP does not cross the alveolar wall. The proportion of trichloracetic acid-precipitable [125I]SAP in the lung tissue or lavage did not change as a function of time. These data are evidence that the instilled [125I]SAP is not degraded. To control for possible non-specific uptake of protein, lungs of neonatal rabbits were instilled with [125I]-rabbit serum albumin, a protein abundant in alveolar fluid. Less than 3% of the [125I] albumin was taken up by the lung tissue after 1 hr. We have shown that the surfactant apoprotein is taken up by the lung, and thus may be involved in the process of surfactant reutilization.

Phospholipid binding and biophysical activity of pulmonary surfactant-associated protein (SAP)-35 and its non-collagenous COOH-terminal domains.

Surfactant-associated protein of Mr = 35,000, SAP-35, is the major glycoprotein present in mammalian pulmonary surfactants. In this study, canine SAP-35 and several of its COOH-terminal peptides were purified and characterized by amino acid composition and NH2-terminal sequencing analysis. These proteins were then studied in terms of their specific lipid-binding characteristics and surface activity when combined with a synthetic phospholipid mixture, SM, chosen as an approximation of lung surfactant phospholipids. Purified, delipidated SAP-35 bound SM strongly. In contrast, SAP-21 (a non-collagenous fragment generated by collagenase digestion) bound phospholipid weakly; SAP-18 (an acidic COOH-terminal fragment comprising residues Gly-118 to Phe-231) did not bind phospholipid, demonstrating the importance of hydrophobic amino acid residues Gly-81 to Val-117 and the NH2-terminal collagenous domain in interaction of the SAP-35 with phospholipids. In surface activity experiments, purified SAP-35 enhanced the adsorption of SM phospholipids in terms of both rate and overall surface tension lowering. However, the adsorption facility of the SM-SAP-35 mixture did not approach that of either whole surfactant or the surfactant extract preparations, calf lung surfactant extract or surfactant-TA, used in exogenous surfactant replacement therapy for the neonatal respiratory distress syndrome. In addition, the dynamic surface activity of the SM-SAP-35 mixture was well below that of natural surfactant or surfactant extracts. This was also true of mixtures of SM phospholipids combined with the SAP-18 and SAP-21 fragments of SAP-35.

Effect of Choline Deficiency on Lung Phospholipid Concentrations in the Rat

Lung surfactant and nonsurfactant phospholipid concentrations were analyzed in relation to choline status in male rats fed a choline-deficient (CD) or choline-supplemented (CS) diet over an 8-d period. On the first day plasma choline concentrations were significantly lower (11.5 ± 0.9 µM) in rats fed the CD diet than in those fed the CS diet (16.1 ± 1.2 µM). This relationship continued for the duration of the study. Hepatic phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratios were significantly lower after d 1 of the CD diet, further decreased on d 2 (1.09 ± 0.04) and remained low through d 8. Only on d 4 were lung surfactant PC and total phospholipid concentrations lower in rats fed the CD diet than in those fed the CS diet. The composition of surfactant, determined by the ratio of PC to total phospholipids, did not change. On both d 4 and d 8 the PC/PE ratios in the non-surfactant fraction were lower in rats fed the CD diet than in those fed the CS diet. This shift in PC/PE ratio in the lung is similar to the PC/PE shift in the liver associated with dietary choline deficiency. The altered lung phospholipid concentrations in the nonsurfactant (residual) fraction on d 4 and d 8 suggest an adaptation in the lung’s phospholipid metabolism to replenish the physiologically essential surfactant PC.

Developmental aspects of lung lipids.

From this review, it is evident that multiple maternal/fetal endogenous or completely exogenous factors have been associated with the complex process regulating fetal lung development. Recent in vitro experiments with human fetal lung explants are especially noteworthy and may establish a perspective for future research. Snyder et al (108) and Medelson et al (74) have found that lung explants from 16-22-week abortuses show differentiated type II cells and augmented PC synthesis within 4 days of culture, rather than the minimum 10- to 15-week period expected in utero. Such a phenomenon is reminiscent of the usual time for clinical recovery from uncomplicated RDS (34). Thus, although expression of the genes influencing lung surfactant phospholipid synthesis and related biochemical processes normally occurs relatively late in gestation, the potential for biochemical differentiation is clearly present in earlier stages. It appears then that the "programming" of the fetal lung for maturation is not absolute but may be altered under certain influences. Whether the advent of lung biochemical maturation occurs as a result of release from inhibition, as the human lung explant data imply, or occurs in response to stimuli, as suggested by exogenous corticosteroid effects, remains to be clarified and is a very challenging scientific problem. It will also be of great interest to define further other biochemical regulators, such as fibroblast pneumocyte factor, that may play an important role in fetal lung maturation.

Lung Surfactant Phospholipids as Related to Hydration and Choline Status of Fasted Rats

Hydration status and choline nutrition were evaluated relative to the concentration of lung surfactant phosphatidylcholine (PC) in fasted rats. Rats deprived of food for 72 h showed lower voluntary water consumption and consistently lower levels of both PC and total phospholipid (TPL) present in isolated pulmonary surfactant than ad libitum-fed controls, although the ratio of surfactant PC to TPL and the residual PC and TPL concentrations were not different. Higher hematocrit values observed in the fasted animals were not altered by the administration of water or saline by orogastric tube nor was the low surfactant PC level corrected by fluid therapy. Evidence of choline deficiency was demonstrated in the fasted rats as there was a significant shift in hepatic PC:phosphatidylethanolamine; however, plasma choline levels did not change. The administration to fasted animals of up to 2.4 mmol of choline chloride via the drinking water (containing 60 mM choline) or an orogastric tube did not affect the plasma choline concentrations or the production of lung surfactant PC.

An ethanol/ether soluble apoprotein from rat lung surfactant augments liposome uptake by isolated granular pneumocytes.

Ethanol/ether soluble apoproteins, comprising 17% of the total recovered surfactant-associated proteins, were isolated from rat lung surfactant and purified by silicic acid chromatography. The protein that eluted in 4:1 chloroform/methanol accounted for greater than 85% of protein in the ethanol/ether soluble fraction and was termed surfactant apoprotein Et (Apo Et). By sodium dodecyl sulfate polyacrylamide gel electrophoresis, this protein had an apparent molecular weight of approximately 10,500. Apo Et was evaluated for its effect on uptake of synthetic phospholipids in liposomal form by isolated granular pneumocytes (Type II alveolar epithelial cells) in primary culture. Liposomes were prepared to approximate the phospholipid composition of the alveolar surfactant, and uptake was measured by the accumulation of the radioactively labeled dipalmitoyl phosphatidyl choline fraction. The uptake of liposomal phosphatidylcholine by cells incubated for 2 h with Apo Et was increased by 61% over control. Most of the cell-associated phospholipid uptake was resistant to treatment with trypsin, suggesting an increased internalization of liposomal material in the presence of Apo Et. The effect of Apo Et on uptake was concentration and time dependent and was not associated with cell damage, phospholipase activity, or detergent properties of the protein. Apo Et had no significant effect on phosphatidylcholine uptake by granular pneumocytes maintained for 7 d in primary culture. Apo Et augmented the uptake of phospholipids by alveolar macrophages although total uptake by these cells was less than that observed with granular pneumocytes. Because Apo Et increases the rate of uptake of surfactant phospholipids by alveolar cells (granular pneumocytes and alveolar macrophages), this protein may represent a physiologically important regulator for clearance of lung surfactant phospholipids.

Effect of nutritional status on the lung surfactant system: food deprivation and caloric restriction.

It has been reported that food deprivation may result in decreased synthesis of lung surfactant phospholipids while the ratio of saturated and unsaturated fatty acids of phosphatidylcholine is maintained. To further investigate this effect, rats were deprived of diet for 24, 48, 72, or 96 hr or fed a nutritionally complete but calorie-deficient diet for 48, 96, 144, and 192 hr. The surfactant was separated into extracellular and intracellular fractions, with the remaining lung tissue pooled as a nonsurfactant fraction. The total phospholipids, phosphatidylcholine, phosphatidylglycerol, and disaturated phosphatidylcholine of each surfactant fraction and the remaining lung tissue were analyzed. The data suggest that on a DNA basis, food and caloric deprivation results temporarily in an altered quantity of pulmonary phospholipids. By 96 hr of fasting or 192 hr of calorie-deficient diet, the pool sizes were replenished and no longer significantly different from the control state. In addition, the distribution of phosphatidylglycerol and phosphatidylcholine was modified in extracellular and intracellular surfactant fractions and in the nonsurfactant tissue fraction. Although the percentage of total phospholipids found as phosphatidylcholine was decreased, the relationship between saturated and unsaturated phosphatidylcholine was preserved in the extracellular surfactant fraction. These results demonstrate that during food and caloric deprivation, the lung quickly adapts to maintain the quality and quantity of surfactant on the alveolar surface.

The effect of betamethasone and fetal sex on the synthesis and maturation of lung surfactant phospholipids in rabbits

In the present study we investigated the maturation of the surfactant phospholipids and the role of fetal sex on the effect of betamethasone in male and female rabbit fetuses. Betamethasone was administered to the doe (0.2 mg/kg intramuscularly) 42 and 18 h prior to killing. The fetuses were studied at 27 and 28 days from conception. Results from the alveolar lavage show that male fetuses tended to have a lower disaturated phosphatidylcholine/sphingomyelin ratio and lower levels of phosphatidylinositol. Phosphatidylglycerol was detected in trace amounts. This was apparently due to the high extracellular levels of myo-inositol inhibiting the synthesis of surfactant phosphatidylglycerol while increasing the synthesis of surfactant phosphatidylinositol. Betamethasone increased the recovery of disaturated phosphatidylcholine and phosphatidylinositol from the lung lavage in both sexes. As studied in lung slices in vitro, the betamethasone treatment decreased the incorporation of glucose into phospholipids, including into the fatty acid moiety of disaturated phosphatidylcholine, although it had no significant effect on the incorporation of glucose into the glycerol moiety of disaturated phosphatidylcholine. However, the addition of palmitate increased the incorporation of glucose into the glycerol moiety of disaturated phosphatidylcholine. The betamethasone treatment did not increase the incorporation of [1- 14C]pyruvate into disaturated phosphatidylcholine. Following betamethasone administration, the availability of fatty acids may become rate-limiting for the synthesis of surfactant phospholipids. Betamethasone increased the activities of phosphatidic acid phosphohydrolase and phosphatidate cytidyltransferase in a fraction of microsomal membranes. The present evidence suggests that the glucocorticoid-induced lung maturation and the maturation of the normal lung are associated with an increase in the activity of the enzymes which are involved in metabolizing phosphatidic acid to neutral and acidic surfactant phospholipids. Furthermore, this study demonstrated that the delay in the maturation of the surfactant secretion of the male fetus was not explained by possible sex-related differences in the biosynthesis of the phospholipids.

Role of an acidic compartment in synthesis of disaturated phosphatidylcholine by rat granular pneumocytes.

A possible role for an acidic subcellular compartment in biosynthesis of lung surfactant phospholipids was evaluated with granular pneumocytes in primary culture. Incubation with chloroquine (100mum) was used to perturb this compartment. With control cells, incorporation of [9,10-(3)H]palmitic acid into total lipids and into total phosphatidylcholines increased linearly with time up to 4h. Total incorporation into phosphatidylcholine during a 1h incubation was 999+85pmol of [9,10-(3)H]palmitic acid, 458+/-18pmol of [1-(14)C]oleic acid and 252+/-15pmol of [U-(14)C]glucose per mug of phosphatidylcholine phosphorus. The cellular content of either disaturated phosphatidylcholine or total phosphatidylcholines did not change during a 2h incubation with chloroquine. In the presence of chloroquine, the specific radioactivity of [(3)H]palmitic acid in disaturated phosphatidylcholine increased by 40%, and that of disaturated-phosphatidylcholine fatty acids from [U-(14)C]glucose increased by 125%. Incorporation of [1-(14)C]oleic acid into phosphatidylcholine was decreased by chloroquine by 79% and 33% in the presence or absence of palmitic acid respectively. Chloroquine stimulated phospholipase activity in intact cells, and in sonicated cells at pH4.0, but not at pH8.5. The observations indicate that chloroquine stimulates synthesis of disaturated phosphatidylcholine in granular pneumocytes from fatty acids, both exogenous and synthesized de novo, which can be due to stimulation of acidic phospholipase. This stimulation of acidic phospholipase A activity by chloroquine appears to be coupled to the synthesis of disaturated phosphatidylcholine, thereby enhancing remodelling of phosphatidylcholine synthesized de novo. Our findings, therefore, implicate the involvement of an acidic subcellular compartment in the remodelling pathway of disaturated phosphatidylcholine synthesis by granular pneumocytes.

Source of lung surfactant phospholipids: comparison of palmitate and acetate as precursors.

The phospholipids and the fatty acid compositions of major phospholipids in rat lung parenchyma, microsomes, lamellar bodies and alveolar wash were quantified. Adult rats were injected simultaneously with [3H]palmitate and [14C]acetate into the femoral vein. The appearance of labeled phosphatidylcholine (PC), desaturated phosphatidylcholine (DSPC) and phosphatidylglycerol (PG) in each lung fraction was measured during short periods of time (5 min to 2 hr) after isotope administration. Relatively more PC, DSPC and PG labeled with acetate radioactivity in lung microsomes entered lamellar body and alveolar wash fractions than those labeled with palmitate radioactivity. However, there was no difference between palmitate and acetate labeled phospholipids in the transport from microsomes to lamellar bodies by phospholipid exchange proteins. On the other hand, prior injection of colchicine resulted in decrease in the transport of PC from microsomes to alveolar space to a relatively greater extent in the acetate radioactivity than in the palmitate radioactivity.

Effects of maternal insulin or glucose infusion on the fetus: Study on lung surfactant phospholipids, plasma myoinositol, and fetal growth in the rabbit

Pregnant rabbits were given continuous intravenous insulin between days 26.7 and 28.7 after conception. The treatment decreased fetal serum glucose, insulin, and myoinositol. Furthermore, maternal insulin decreased fetal growth slightly, and improved the survival of the prematurely delivered fetuses. Analysis of phospholipids recovered by alveolar lavage revealed that the lung surfactant was quantitatively and qualitatively superior to the surfactant from the fetuses of the saline-glucose control animals. This effect on the lung was more striking than that of glucocorticoid. Another group of pregnant rabbits received continuous intravenous glucose between days 27.0 and 29.0 after conception. The hyperinsulinemic fetuses of the glucose-infused does weighed more and had higher serum glucose and myoinositol than did those of the control animals. There was no detectable difference in alveolar lavage phospholipids between hyperinsulinemic and normoinsulinemic fetuses of glucose-infused does. The possible importance of these findings in understanding the mechanism of acceleration of lung maturation is discussed.

Determination of phosphatidylglycerol in amniotic fluid by a simple one-dimensional thin-layer chromatography method

Phosphatidylglycerol (PG) in amniotic fluid is the second important component of lung surfactant phospholipids and may be clinically useful in assessing fetal lung maturity in utero. Although methods for PG determination are available, there are shortcomings in clinical application. We developed an alternative reliable onedimensional thin-layer chromatography (TLC) method for separating and quantitating PG in amniotic fluid. A mini-TLC plate (8 × 10 cm) was prepared from silica gel H containing 5% ammonium sulfate. The plate was first developed in tetrahydrofuron/dimethoxymethane/methanol/2N ammonium hydroxide (30.0:20.6:5.6:3.0, v/v) and then in chloroform/methanol (60:9, v/v) in the same direction. PG was clearly separated from other phospholipids and neutral lipids, even when large amounts of other phospholipids were present on the TLC plate. The density of the charred PG was directly proportional to the amount of PG up to 8 nmol. The content of PG in nmol in the specimen can be quantitated by comparing with a standard PG. Up to 10% of blood serum or 3% meconium showed no detectable PG, nor did these substances affect PG quantitation in amniotic fluid. This method is sensitive and accurate. It is also time-saving and economical.

Analysis of labeling and clearance of lung surfactant phospholipids in rabbit. Evidence of bidirectional surfactant flux between lamellar bodies and alveolar lavage.

Turnover and clearance of lung surfactant phospholipids were studied with particular reference to myoinositol-induced perturbation in the acidic phospholipids. Administration of myoinositol decreased [(3)H]palmitate and [(32)P]phosphate incorporation into phosphatidylglycerol by 80-90% in whole lung, and by 94-99% in lamellar bodies and in alveolar lavage. The increased incorporation of radioactive isotopes into phosphatidylinositol following myoinositol, was inverse to the decrease in phosphatidyl-glycerol incorporation. Myoinositol treatment affected neither content nor labeling of phosphatidylcholine or disaturated phosphatidylcholine as studied within 50 h of administration. Phosphatidylglycerol was pulse labeled by intravenous [(32)P]phosphate and [(3)H]palmitate, followed by myoinositol. The biological half-lives of phosphatidylglycerol in the microsomal fraction, lamellar bodies, and alveolar lavage were 1.6, 4.6, 5.4 h (with (3)H), and 2.8, 6.5, 7.0 h (with (32)P), respectively.(32)P-labeled lung surfactant tracer was applied to the airways in saline suspension and the clearance of phospholipid radioactivity was measured in alveolar lavage, alveolar macrophages, lamellar bodies and lung homogenates. The clearance rates of phosphatidylcholine, disaturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylinositol as studied in whole lung over 6 h were 3.4-5.8% h. Only a small amount of phospholipid radioactivity was recovered in the alveolar macrophage fraction (including bis-[monoacylglycerol]phosphate). Phospholipid radioactivity in alveolar lavage fell to 40-70% of the maximum during the 1st h, and to 5-18% over the next 6 h. During 2 h after the application of phospholipids, the radioactivity in the lamellar body fraction increased, and the specific radioactivities approached those in alveolar lavage. The association of phosphatidylglycerol with lamellar bodies was unaffected by myoinositol. Phosphatidylinositol entered more slowly than did phosphatidylglycerol from microsomes to the alveolar lavage fraction, and from alveolar lavage to lamellar bodies. These differences may be of importance regarding the poor performance of phosphatidylinositol-containing surfactant at birth. Further investigations are needed to clarify the possible role for the postulated bidirectional surfactant flux between the lamellar body and alveolar lavage fractions in maintaining the activity of surfactant.

Phospholipid synthesis in fetal lung organotypic cultures and isolated type II pneumocytes

Type II pneumocytes from fetal rabbit lungs were grown in an organotypic system and used to study surfactant phospholipid synthesis. This organotypic system was further employed as a means for isolating purified type II cells which were grown in monolayer cultures. Phospholipid synthetic properties for these purified type II cells at different stages of culture were studied using the radioactively labeled substrates: palmitate, choline and acetate. Additionally, fibroblasts were recovered from the organotypic system and grown in isolated cultures or in combination with type II cells. A comparison of the phospholipid composition and biosynthesis for these cell preparation indicated that in all instances, with the exception of fetal lung fibroblasts, the cultures were capable of producing saturated phosphatidylcholine as a major phospholipid product. The relative molar incorporation into phospholipids for the substrates studied differed depending on the type cell preparation being examined. The formation of surfactant phospholipids appeared most similar for the organotypic system and mixed fibroblast/type II cell preparations. Furthermore, a mixed culture of fibroblasts and type II cells produced larger proportions of surfactant phospholipids than type II cells alone. These observations indicate that the organotypic system is a useful model for examining fetal lung surfactant phospholipid synthesis and may also be employed as a simple means for isolating fetal type II pneumocytes.

Fetal rat lung phosphatidylcholine synthesis in diabetic and normal pregnancies: A comparison of prenatal dexamethasone treatments

The effects of maternal diabetes upon fetal lung surfactant phospholipid metabolism were studied using 19-day gestational age fetal rats from mothers with streptozotocin-induced diabetes mellitus. In this experimental animal model, maternal glucose intolerance significantly impaired fetal body and lung development. However, incorporation of [ 14C]palmitate and [ 3H]choline into lung total and disaturated phosphatidylcholine was unimpaired in offspring of diabetic mothers. Dexamethasone, which is known to promote fetal lung maturation in normal pregnancies, was administered to diabetic and control mothers during late gestation. Prenatal dexamethasone inhibited lung growth in both diabetic and control pregnancies. While this agent slightly stimulated [ 14C]palmitate incorporation into total phosphatidylcholine and markedly enhanced [ 3H]choline incorporation into both disaturated and total phosphatidylcholine in control pregnancies, it failed to stimulate incorporation of either precursor into fetal lung from diabetic pregnancies.

Protein and lipid-protein fractions of lung washings: chemical characterization.

ArticleProtein and lipid-protein fractions of lung washings: chemical characterization.G Colacicco, A R Buckelew Jr, and E M ScarpelliG Colacicco, A R Buckelew Jr, and E M ScarpelliPublished Online:01 Jun 1973https://doi.org/10.1152/jappl.1973.34.6.743MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPulmonary Surfactant23 October 2019Biological Processes and ReactionsA new method for measurement of surfactant specific apoprotein in amniotic fluid13 April 2004 | International Journal of Gynecology & Obstetrics, Vol. 29, No. 2Surface‐tension measurements of pulmonary lavage from ozone‐exposed ratsJournal of Toxicology and Environmental Health, Vol. 19, No. 1Development and Growth of the Human Lung1 January 2011Lipid Synthesis and Surfactant Turnover in the Lungs1 January 2011Arguments against and alternatives for an extracellular surfactant layer in the alveoli of mammalian lungJournal of Theoretical Biology, Vol. 114, No. 4Glycolipid accumulation in bronchoalveolar space in adult respiratory distress syndrome.Journal of Lipid Research, Vol. 25, No. 11Immunohistochemical techniques and their applications in the histopathology of the respiratory system.Environmental Health Perspectives, Vol. 56Organotypic culture of fetal lung type II alveolar epithelial cells: applications to pulmonary toxicology.Environmental Health Perspectives, Vol. 56Introduction: Lung Surfactant—Phospholipids and Apoproteins2 July 2009 | Experimental Lung Research, Vol. 6, No. 3-4Quantification of an apoprotein of pulmonary surfactant in normal and alloxan-induced diabetic rats by electroimmunoassayLung, Vol. 161, No. 1Bronchoalveolar Fluid and Subcellular Surfactant FractionsThe Composition of Pulmonary SurfactantExperimental studies on the pulmonary surfactant. Reconstitution of surface-active material.Journal of Lipid Research, Vol. 23, No. 1Analysis of pulmonary surfactant apoproteins by electrophoresisBiochimica et Biophysica Acta (BBA) - Protein Structure, Vol. 670, No. 3Isolation of a major apolipoprotein of canine and murine pulmonary surfactant Biochemical and immunochemical characteristicsBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 665, No. 3Surfactant substitution; experimental models and clinical applicationsLung, Vol. 158, No. 1Quantification of surfactant phospholipids in the dog lungJournal of Lipid Research, Vol. 21, No. 8Selective reduction of phosphatidylglycerol and phosphatidylcholine in pulmonary surfactant by 4-aminopyrazolo(3,4d)pyrimidine in the ratJournal of Lipid Research, Vol. 21, No. 8Lung development and the pulmonary surfactant system: Hormonal influencesThe Anatomical Record, Vol. 198, No. 1Extramembranous particles in tubular myelin from rat lungJournal of Ultrastructure Research, Vol. 71, No. 1Type II alveolar cells in organotypic cultureBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 617, No. 2The neutral glyceroglucolipids of alveolar lavage from rabbitBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 574, No. 3Isolation and Characterization of a Sulfated Glyceroglucolipid from Alveolar Lavage of RabbitEuropean Journal of Biochemistry, Vol. 98, No. 1Ultrahistochemical investigations of dog lung surfactant with ruthenium red and iodoplatinate reactionsHistochemistry, Vol. 60, No. 3On the trace of protein moiety in pulmonary surfactantBiochemical Medicine, Vol. 20, No. 1Activation of Alveolar Macrophages Exposed to Lavage-Procured Immunoglobulin G Obtained from Normal Rabbit LungsInfection and Immunity, Vol. 20, No. 2Effect of serum albumin on dynamic force-area curve of dipalmitoyl lecithinRespiration Physiology, Vol. 32, No. 3Pulmonary surfactant: Distribution of lipids, proteins and surface activity in ultracentrifugation of rabbit pulmonary washing and derived fractionsLipids, Vol. 12, No. 11Effects of cholesterol and cholesteryl ester on dynamic surface tension of dipalmitoyl lecithinJournal of Colloid and Interface Science, Vol. 61, No. 3Purification of surfactant from lung washings and washings contaminated with blood constituentsLipids, Vol. 12, No. 6Morphological aspects of type II alveolar pneumocytes following treatment with puromycin in vivoAmerican Journal of Anatomy, Vol. 148, No. 2Pulmonary lipid biosynthesis: Simultaneous double-label in lipids from plasma, lung tissue and surfactant using a dog heart-lung preparationInternational Journal of Biochemistry, Vol. 8, No. 7Isolation and Characterization of Proteins Associated with the Lung Surfactant System5 March 2007 | Preparative Biochemistry, Vol. 7, No. 6Structure of the phosphatidylcholines of the lung surfactant at birth in normal full term infantsClinica Chimica Acta, Vol. 71, No. 3Pulmonary surfactant: A surface chemistry viewpointAnnals of Biomedical Engineering, Vol. 3, No. 2Characterization of lung surfactant: factors promoting formation of artifactual lipid-protein complexesJournal of Lipid Research, Vol. 16, No. 3Relationship between Intra- and Extracellular Surface-Active Fractions from Rat LungsChest, Vol. 67, No. 2Lung surfactantBiochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, Vol. 344, No. 3-4The identification of phosphatidylglycerol in the rat, rabbit, monkey and human lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 360, No. 1Extrapulmonary source of amniotic fluid phospholipidsAmerican Journal of Obstetrics and Gynecology, Vol. 118, No. 6Pulmonary Surfactants: Molecular Structure and Biological Activity More from this issue > Volume 34Issue 6June 1973Pages 743-9 https://doi.org/10.1152/jappl.1973.34.6.743PubMed4123102History Published online 1 June 1973 Published in print 1 June 1973 Metrics

Rapid incorporation of palmitate into lung: site and metabolic fate.

ArticleRapid incorporation of palmitate into lung: site and metabolic fate.H K Darrah, and J Hedley-WhyteH K Darrah, and J Hedley-WhytePublished Online:01 Feb 1973https://doi.org/10.1152/jappl.1973.34.2.205MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByLung Lipid Composition and Surfactant BiologyIncreased palmitoyl-myristoyl-phosphatidylcholine in neonatal rat surfactant is lung specific and correlates with oral myristic acid supplyWolfgang Bernhard, Marco Raith, Christopher J. Pynn, Christian Gille, Guido Stichtenoth, Dieter Stoll, Erwin Schleicher, and Christian F. Poets1 August 2011 | Journal of Applied Physiology, Vol. 111, No. 2Myristate is selectively incorporated into surfactant and decreases dipalmitoylphosphatidylcholine without functional impairmentChristopher J. Pynn, M. Victoria Picardi, Tim Nicholson, Dorothee Wistuba, Christian F. Poets, Erwin Schleicher, Jesus Perez-Gil, and Wolfgang Bernhard1 November 2010 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 299, No. 5Influence of dexamethasone on the lipid distribution of newly synthesized fatty acids in fetal rat lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 1005, No. 3Activity of long chain acyl-CoA synthetase in isolated alveolar type II cellsBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 918, No. 1Experimental studies on myocardial metabolism of iodinated fatty acids: a proposal for a new curve analysis techniqueLung surfactantProgress in Lipid Research, Vol. 26, No. 3Development and Growth of the Human Lung1 January 2011Lung Cell Biology1 January 2011General Enzymology of the LungPhospholipid composition of guinea pig lung lavageLipids, Vol. 20, No. 1Purification and Characterization of Fatty Acid Binding Protein in Mammalian Lung2 July 2009 | Experimental Lung Research, Vol. 9, No. 1-2Pulmonary macrophage: a major source of lipoprotein lipase in the lungBiochemical and Biophysical Research Communications, Vol. 125, No. 1Pentose pathway of glucose metabolism in isolated granular pneumocytesBiochemical Pharmacology, Vol. 33, No. 8Source of lung surfactant phospholipids: Comparison of palmitate and acetate as precursorsLipids, Vol. 17, No. 12Metabolic fate of fatty acids in type II cells isolated from adult rat lungLung, Vol. 160, No. 1Lung Cell Culture SystemsPathways of Palmitate Metabolism in the Isolated Rat Lung2 July 2009 | Experimental Lung Research, Vol. 2, No. 1Phospholipids of the lung in normal, toxic, and diseased states26 September 2008 | CRC Critical Reviews in Toxicology, Vol. 9, No. 3Quantification of surfactant phospholipids in the dog lungJournal of Lipid Research, Vol. 21, No. 8Effect of alloxan-induced chronic diabetes on lipid composition and lipoprotein lipase activity of rat lungBiochemical Medicine, Vol. 21, No. 2An in vivo comparison of acetate and palmitate as precursors of surfactant phosphatidylcholineBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 572, No. 3Effect of Tobacco Smoke on the Metabolism of Rat LungArchives of Environmental Health: An International Journal, Vol. 34, No. 1The effect of DL-2-bromopalmitate on the utilization of palmitic acid by rat granular pneumocytesVirchows Archiv B Cell Pathology, Vol. 29, No. 1Labeling of phospholipids in the surfactant and subcellular fractions of rabbit lung.Journal of Biological Chemistry, Vol. 253, No. 11Lung Maturity and Pulmonary Phospholipid MetabolismThe labeling and biological half-life of phosphatidylcholine in subcellular fractions of rabbit lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 489, No. 3Role of lamellar bodies in the biosynthesis of phosphatidylcholine in mouse lungBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 488, No. 2Normal and pathologic biochemistry of the lung.Environmental Health Perspectives, Vol. 16Role of lamellar inclusions in surfactant production: studies on phospholipid composition and biosynthesis in rat and rabbit lung subcellular fractions.Journal of Lipid Research, Vol. 16, No. 6Lungenstoffwechsel bei SchocklungeLipoprotein lipase in rat lung the effect of fastingBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 380, No. 1 More from this issue > Volume 34Issue 2February 1973Pages 205-13 https://doi.org/10.1152/jappl.1973.34.2.205PubMed4739324History Published online 1 February 1973 Published in print 1 February 1973 Metrics

Dynamic compliance, limit cycles, and static equilibria of excised cat lung.

Dynamic compliance, limit cycles, and static equilibria of excised cat lung.