Characterization of pulmonary surfactant from ox, rabbit, rat and sheep.

1. Pulmonary surfactants from ox, rabbit, rat and sheep were isolated and analysed. 2. All preparations had a high anenoic phosphatidylcholine content and would produce stable surface tensions of 0.01 Nm-1 or less. 3. Protein content was 8-18% of the dry weights. A number of proteins were observed; their overall composition were high in hydrophobic amino acid residues. 4. Lipid content varied from 79% (ox) to 90% (rabbit) with phosphatidylcholine representing from 58% (sheep) to 83% (rabbit) of the total lipid. The surfactant preparations were rather similar in lipid composition except that sheep surfactant contained about 10% lysophosphatidylcholine. 5. Hexadecanoic acid was the principal fatty acid. It was particularly high in phosphatidylcholine. 6. Phosphatidylglycerol was a minor constituent of all surfactants but phosphatidyldimethylethanolamine was not detected.     

The development of surfactant synthesis in fetal rabbit lung organ culture exhibits a sex dimorphism

Sex differences in amniotic fluid and lung lavage surfactant have been found. Although these studies suggest that augmented fetal surfactant synthesis occurs earlier in the female fetus, there is little direct evidence for a sex difference in fetal surfactant synthesis. We studied the synthesis of surfactant by evaluating the appearance of labelled phospholipids in lamellar bodies recovered from sex-specific organ culture of fetal rabbit lungs. Furthermore, we studied the ability of dexamethasone to stimulate surfactant synthesis in male and female fetal lungs. Organ culture was begun on day 21 of gestation. After 5 days the incorporation of [1,3-14C]glycerol into phosphatidylcholine (PC), disaturated phosphatidylcholine, phosphatidylinositol (PI), and phosphatidylglycerol was studied. Female lungs in organ culture synthesized more disaturated PC per milligram protein than male lungs. In the presence of dexamethasone (10(-8) M) and dihydrotestosterone (10(-8) M) an increased synthesis was noted in the female cultures of PC (270%), disaturated PC (234%), PI (281%), and phosphatidylglycerol (754%). No significant increase in the synthesis of PC or disaturated PC was observed in the male cultures. However in the male cultures smaller increases in the synthesis of PI (193%) and of phosphatidylglycerol (360%) were observed. Overall, dexamethasone stimulated synthesis in females but not in males such that significant differences in the synthesis of all phospholipids were found in the presence of 10(-8) M dexamethasone. These studies show that the synthesis of surfactant in the fetal lung is sexually dimorphic, as is the ability of dexamethasone to regulate synthesis. An understanding of the mechanism which causes these differences may provide important insight into the control of the developmental clock which regulates the orderly progression of development.     

Phosphatidylglycerol in lung surfactant. II. Subcellular distribution and mechanism of biosynthesis in vitro.

Lamellar inclusion bodies, apparent precursors for alveolar surfactant lining, have remarkably similar phospholipid composition to surfactant from alveolar lavage, but distinctly different from other fractions studied: mitochondria, microsomal fraction containing endoplasmic reticulum membranes, plasma membranes and nuclei. Surfactant contained (as % of total phospholipid phosphate): 75.5-77.0% lecithin, 11.0-11.2% phosphatidylglycerol, 4.2-4.6% phosphatidylethanolamine, 3.0-3.2% phosphatidylinositol, 1.5-1.7% bis-(monoacylglycerol) phosphate, 1.2-1.9% phosphatidylserine, and 0.7-1.5% sphingomyelin. Fatty acids of phosphatidylglycerol from lamellar bodies were similar to those from microsomes but different from those in mitochondria. Lung homogenate in continuous sucrose density gradient displayed two major activity peaks of phosphatidylglycerol synthesis: the heavier from mitochondria; the lighter from endoplasmic reticulum. Studies on mechanism of phosphatidylglycerol synthesis in vitro revealed (in these two fractions) CDP-diglyceride and sn-glycerol phosphate precursors to phosphatidylglycerol phosphate, that hydrolysed to phosphatidylglycerol. In microsomes disaturated CDP-diglycerides were 1.6-1.9 times more active substrates than in mitochondria, whereas CDP-diglycerides from egg lecithin were almost equally active. In contrast to lung mitochondria no cardiolipin synthesis was detected in microsomes. The highest specific activities for phosphatidate cytidyltransferase, CDP-diglyceride-inositol phosphatidyltransferase, choline phosphotransferase, and phosphatidylethanolamine methyltransferase were all found in microsomes. The present in vitro studies and additional evidence (M. Hallman and L. Gluck, (1975) Fed. Proc. 34, 274) support the hypothesis that de novo synthesis of surfactant lecithin phosphatidylinositol and phosphatidylglycerol takes place in the endoplasmic reticulum of alveolar cells.     

Phosphatidylglycerol-deficient lung surfactant has normal properties

We have investigated the effects of substituting phosphatidylinositol (PI) for phosphatidylglycerol (PG) on the functional properties of rabbit lung surfactant. We gave oral 10% glucose solution for 3 days to 11 rabbits and 10% inositol to 12 others. Lung lavage surfactant phospholipids were normal in both groups, except that PG was low and PI was high in the inositol group. Fatty acyl group distributions did not differ, except for a slight decrease of oleic acid in the inositol group. Electron microscopic examination showed normal surfactant structure in both. The time course of surfactant adsorption to an air-water interface was similar in both groups. Minimum surface tension after film compression was 4.0 +/- 0.8 mN . m-1 in the glucose group and 2.9 +/- 1.3 mN . m-1 in the inositol group (mean +/- SE). Surface potential-surface pressure isotherms were identical to within 12 mV. Arterial blood gases breathing air and 100% O2 were the same in both groups, as were pressure-volume curves of excised lungs, with both air and saline filling. The results suggest that, if acidic phospholipids are necessary for maintaining normal surfactant structure and surface properties, normal pressure-volume relationships, and normal gas exchange, then PI may substitute for PG.     

Role of lamellar inclusions in surfactant production: studies on phospholipid composition and biosynthesis in rat and rabbit lung subcellular fractions.

Lamellar inclusion bodies in the type II alveolar epithelial cell are believed to be involved in pulmonary surfactant production. However, it is not clear whether their role is that of synthesis, storage, or secretion. We have examined the phospholipid composition and fatty acid content of rabbit lung wash, lamellar bodies, mitochondria, and microsomes. Phosphatidylcholine and phosphatidylglycerol, the surface-active components of pulmonary surfactant, accounted for over 80% of the total phospholipid in lung wash and lamellar bodies but for only about 50% in mitochondria and microsomes. Phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, and sphingomyelin accounted for over 40% of the total in mitochondria and microsomes but for only 6% in lung wash and 15% in lamellar bodies. The fatty acid composition of lamellar body phosphatidylcholine was similar to that of lung wash, but different from that of mitochondria and microsomes, in containing palmitic acid as a major component with little stearic acid and few fatty acids of chain length greater than 18 carbon atoms. The biosynthesis of phosphatidylcholine and phosphatidylglycerol was examined in the mitochondrial, microsomal, and lamellar body fractions from rat lung. Cholinephosphotransferase was largely microsomal. The activity in the lamellar body fraction could be attributed to microsomal contamination. The activity of glycerolphosphate phosphatidyltransferase, however, was high in the lamellar body fraction, although it was highest in the mitochondria and was also active in the microsomes. These data suggest that the lamellar bodies are involved both in the storage of the lipid components of surfactant and in the synthesis of at least one of those components, phosphatidylglycerol.     

Pulmonary surfactant

Pulmonary surfactant reduces the surface tension of the alveolar air-liquid interface, thereby providing mechanical stability and preventing alveolar atelectasis. More than 50% of surfactant is dipalmitoyl phosphatidylcholine, a material that is capable of reducing the surface tension of the alveolar interface to uniquely low values. The functions of the remaining 25% unsaturated phosphatidylcholines, 5-10% phosphatidylglycerol, 5% cholesterol, and 8-10% protein are unknown. Surfactant is synthesized by alveolar epithelial type II cells and is probably secreted as a lipoprotein complex. Lamellar bodies, which distinguish type II cells, are likely to be intracellular sites of transport of processing. The catabolism of surfactant after it is secreted into the alveolar lumen is complicated and involves different turnover times for the phosphatidylcholines, phosphatidylglycerol, and the proteins. The metabolic events are under hormonal control and may involve an interplay between beta-adrenergic agonists cAMP, and prostaglandins. In disease, such as the neonatal and adult respiratory distress syndromes, derangements in the metabolic processes may produce surfactant that is abnormal with respect to its chemical and physical properties.     

The development of the pulmonary surfactant system in California sea lions

Pulmonary surfactant has previously been shown to change during development, both in composition and function. Adult pinnipeds, unlike adult terrestrial mammals, have an altered lung physiology to cope with the high pressures associated with deep diving. Here, we investigated how surfactant composition and function develop in California sea lions (Zalophus californianus). Phosphatidylinositol was the major anionic phospholipid in the newborn, whereas phosphatidylglycerol was increased in the adult. This increase in phosphatidylglycerol occurred at the expense of phosphatidylinositol and phosphatidylserine. There was a shift from long chain and polyunsaturated phospholipid molecular species in the newborn to shorter chain and mono- and disaturated molecular species in the adult. Cholesterol and SP-B concentrations were also higher in the adult. Adult surfactant could reach a lower equilibrium surface tension, but newborn surfactant could reach a lower minimum surface tension. The composition and function of surfactant from newborn California sea lions suggest that this age group is similar to terrestrial newborn mammals, whereas the adult has a "diving mammal" surfactant that can aid the lung during deep dives. The onset of diving is probably a trigger for surfactant development in these animals.     

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 secretion of the male fetus was not explained by possible sex-related differences in the biosynthesis of the phospholipids.     

Quantification of surfactant pool sizes in rabbit lung during perinatal development

Methods are presented for the quantitative isolation of surfactants from fetal and newborn rabbit alveolar lavage returns and post-lavaged lung tissue homogenates. The phospholipid content of both fractions progressively increased between 27 days gestation and term (31 days). The tissue-stored fraction increased approximately 16-fold (from 0.48 +/- 0.13 to 7.83 +/- 0.86 mg/g dry lung) and the alveolar fraction more than 30-fold (from 0.08 +/- 0.02 to 2.69 +/- 0.52 mg/g dry lung). Developmental changes in phospholipid composition were also observed. Tissue-stored surfactant was prepared using differential and density gradient centrifugation. Alveolar surfactant was isolated during fetal development as a high-speed pellet following a one-step differential centrifugation. There was little change in the phospholipid content of fetal alveolar lavage supernatant (range 0.12 +/- 0.04 to 0.28 +/- 0.09 mg/g dry lung). By the first postnatal day the phospholipid content of both lavage fractions significantly increased (pellet, 7.51 +/- 1.79; supernatant, 4.01 +/- 1.36 mg/g dry lung) and both were identified as surfactant. This increase in alveolar surfactant was accompanied by an approximately twofold decrease (to 3.81 +/- 1.1 mg/g dry lung) in the tissue-stored fraction. These data provide a quantitative profile of surfactant accumulation and secretion in developing rabbit lung.     

Regulation and location of phosphatidylglycerol and phosphatidylinositol synthesis in type II cells isolated from fetal rat lung

• 1.1. myo-Inositol decreases the synthesis of phosphatidylglycerol by type II cells isolated from fetal rat lung. Inositol addition also increases the synthesized amount of surfactant phosphatidylinositol. These observations indicate that at least part of the decreasing effect of inositol on phosphatidylglycerol formation is the result of competition between phosphatidylglycerol and phosphatidylinositol synthesis for a common pool of CDPdiacylglycerol.
• 2.2. Studies on the subcellular localization of enzymes measured under optimal conditions suggested that the enzymic activity required for the formation of phosphatidylglycerol is located mainly in the mitochondria, but most likely also for a small part in the endoplasmic reticulum, while the enzymic activity required for phosphatidylinositol formation is located in the endoplasmic reticulum.
• 3.3. Inositol was found to inhibit glycerolphosphate phosphatidyltransferase in the microsomal fraction but not in the mitochondrial fraction derived from the type II cells, indicating that the competition between phosphatidylglycerol and phosphatidylinositol synthesis for CDPdiacylglycerol takes place in the endoplasmic reticulum.
• 4.4. This latter observation together with the observation of a switch-over from surfactant phosphatidylinositol to phosphatidylglycerol production around term indicate that the endoplasmic reticulum is the intracellular site of surfactant phosphatidylglycerol production.

     

Lack of change in the composition of fetal lamb lung surfactant during gestation

Fetal surfactant from lamb lung fluids collected daily from day 114 to day 146 of gestation, was isolated by centrifugation (pellet material) and further purified by sucrose density gradient centrifugation. The concentration of the pellet material from lung fluid (crude surfactant) increased from day 125 till day 135 and fluctuated strongly from that period onwards, whereas lung fluid secretion increased linearly until a few days before parturition. The pellet phospholipid composition changed with gestational age, suggesting biochemical maturation of the surfactant-producing system. The purified surfactant fraction, of which approximately 85% was phosphatidylcholine, did not change however from day 122 onwards except for a small increase in the percentage of phosphatidylglycerol. Alveolar wash surfactant or the lamellar body material, isolated from fetal lungs at different gestational ages had the same composition as surfactant from lung fluids. Only the composition of lamellar bodies of '125 day' lungs differed slightly from that of the lung fluid surfactant. The similar characteristics of all purified surfactant fractions throughout gestation indicate that, in the fetal lamb, lung maturation is associated with an increase in surfactant production no significant changes in phospholipid composition.     

Induction and characterization of the major surfactant apoprotein during rabbit fetal lung development

Antibodies directed against the major apoprotein associated with rabbit lung surfactant were used to characterize the induction and cellular localization of this protein during rabbit fetal lung development. In lung tissues from rabbits of 26 days gestational age and older, discrete epithelial type II cells were stained positively using the peroxidase antiperoxidase technique. The content of the major protein in homogenates of fetal lung tissue was analyzed using an immunoblotting technique. A protein of about 29 kDa, pI less than or equal to 5.6, was first detectable in fetal lung tissue on day 24 of gestation. The 29-36 kDa, mature form of the surfactant apoprotein was first detectable in lung homogenates from 30-day gestational age fetal rabbits. Treatment of homogenates of day 26 and 31 fetal lung tissues with endoglycosidase F, yielded, in both cases, an immunoreactive triplet with more neutral isoelectric points than the proteins in the untreated homogenates. By immunoblot analysis, we found that only the 29-36 kDa, mature form of the surfactant apoprotein was present in lamellar bodies purified from lung tissues of fetuses of 28 and 31 days and from day 2 neonates. These findings are suggestive that only the mature, 29-36 kDa form of the surfactant apoprotein is associated with lamellar bodies during fetal lung type II cell differentiation in vivo.     

A captive bubble method reproduces the in situ behavior of lung surfactant monolayers

We tested a new captive bubble surface tensiometer with films adsorbed from aqueous suspensions of rabbit lung surfactant and a bovine lung surfactant lipid extract and with films of dipalmitoyl-sn-3-glycerophosphorylcholine (DPPC) spread from solvents. The lack of tubes penetrating the bubble surface eliminated potential leakage pathways for the surface film, which was compressed by increasing external pressure. Surface tensions and areas were calculated directly from bubble shapes without the need of pressure measurements. After only one to two compressions, the rabbit surfactant films exhibited the low surface tension, collapse rates, and compressibilities characteristic of the alveolar surface in situ and approached the behavior of spread DPPC films. The bubble "clicking" phenomenon described earlier by Pattle (Proc. R. Soc. Lond. B Biol. Sci. 148: 217-240, 1958) was also reproduced, but only with the bovine extract, which did not perform as well as the rabbit surfactant in surface tests. These findings suggest that surfactant apoprotein SP-A, which was probably present in the rabbit but not the bovine preparations, enhances both adsorption and stability of pulmonary surfactant monolayers.     

Normal surface properties of phosphatidylglycerol-deficient surfactant from dog after acute lung injury

Lung surfactant was isolated from bronchoalveolar lavage of dogs during the late phase of recovery (15 days) from acute alveolar injury induced by subcutaneous injection of N-nitroso-N-methylurethane. This surfactant was compared with surfactant from control dogs in terms of in vitro surface properties, phospholipid composition and protein content, and those of its subfractions. Phospholipid composition and protein content were similar in the two groups, except that phosphatidylglycerol (PG) was markedly reduced and phosphatidylinositol (PI) was increased in the experimental group. In both, isopycnic densities of their subfractions in continuous sucrose density gradient were identical. The time course of surfactant adsorption was similar in both groups. Minimum surface tension (gamma min) was 4.1 +/- 1.5 dynes/cm in the experimental dogs and 3.8 +/- 1.3 dynes/cm in the controls. Surface compressibility (SC), stability index (SI), and dynamic respreadability (DR) of the surfactants from the two groups were nearly identical. When compared to an artificial surfactant composed of dipalmitoyl phosphatidylcholine (DPPC) and PG in 9:1 molar ratio a mixture of DPPC-PI 9:1 prepared identically showed similar gamma min, SC, SI, and DR, and a much higher surface adsorption rate. These results suggest that PG is not essential for normal in vitro surfactant function and that its role may be assumed by PI.     

Pre- and postnatal stimulation of pulmonary surfactant protein D by in vivo dexamethasone treatment of rats.

Fetal (days 18 and 20 of gestation), neonatal (days 0, 2 and 4 of neonate) and adult rats were injected with dexamethasone (1 mg/kg) in vivo and 24 hours later the effect on the contents of surfactant protein D (SP-D) in the rat lungs were examined in comparison with surfactant protein A, disaturated phosphatidylcholine and phosphatidylglycerol. In vivo dexamethasone treatment resulted in significant increases of SP-D content as the other 3 components of surfactant in both fetuses and neonates, but not in adults. Responsiveness to glucocorticoid treatment on SP-D content was maximum on day 1 of neonate (2.7 times control value). The contents of surfactant components examined tend to respond better to steroid in postnatal rats. These data demonstrated that glucocorticoid treatment in vivo for short durations exhibits the stimulatory effect on the contents of SP-D in the fetal and neonatal rat lungs.     

Changes in pulmonary surfactant during bacterial pneumonia

In pneumonia, bacteria induce changes in pulmonary surfactant. These changes are mediated by bacteria directly on secreted surfactant or indirectly through pulmonary type II epithelial cells. The bacterial component most likely responsible is endotoxin since gram-negative bacteria more often induce these changes than gram-positive bacteria. Also, endotoxin and gram-negative bacteria induce similar changes in surfactant. The interaction of bacteria or endotoxin with secreted surfactant results in changes in the physical (i.e. density and surface tension) properties of surfactant. In addition, gram-negative bacteria or endotoxin can injure type II epithelial cells causing them to produce abnormal quantities of surfactant, abnormal concentrations of phospholipids in surfactant, and abnormal compositions (i.e. type and saturation of fatty acids) of PC. The L/S ratio, the concentration of PG, and the amount of palmitic acid in PC are all significantly lower. The changes in surfactant have a deleterious effect on lung function characterized by significant decreases in total lung capacity, static compliance, diffusing capacity, and arterial PO₂ and a significant increase in mean pulmonary arterial pressure. Also decreased concentrations of surfactant or an altered surfactant composition can result in the anatomic changes commonly seen in pneumonia such as pulmonary edema, hemorrhage, and atelectasis.Abbreviations BAL Bronchoalveolar lavage - LPS lipopolysaccharide - PC phosphatidylcholine - PG phosphatidylglycerol - PE phosphatidylethanolamine - PI phosphatidylinositol - PS phosphatidylserine - LPC lysophosphatidylcholine - SPH sphingomyelin - DPPC dipalmitoylphosphatidylcholine - L/S lecithin/sphingomyelin     

Stimualtion of glycerolphosphate phosphatidyltransferase activity in fetal rabbit lung by cortisol administration.

Phosphatidylglycerol is an important component of pulmonary surfactant. Previous studies have shown that direct administration of corticosteroids of thyroxine to the fetus during the latter part of gestation results in accelerated lung maturation with increased surfactant production. We have shown that administration of cortisol to fetal rabbits at 24 days' gestation results 3 days later in a significant increase in the activity of pulmonary glycerolphosphate phosphatidyltransferase, an enzyme involved in the synthesis of phosphatidylglycerol. The activity of the liver enzyme was not affected. Choline phosphotransferase, CDPdiglyceride-inositol phosphatidyltransferase, lysophosphatidic acid acyltransferase and lysolecithin acyltransferase activities were not altered significantly by cortisol treatment. Thyroxine treatment had no effect on any of the enzymes of phospholipid or fatty acid biosynthesis studied.     

Effect of cortisol on the synthesis of lamellar body glycerophospholipids in fetal rabbit lung tissue in vitro

The effect of cortisol on the rate of choline incorporation into tissue phosphatidylcholine was investigated in lung explants from fetal rabbits of 19-28 days gestational age. The explants were incubated in medium with or without fetal calf serum for up to 7 days. When lung tissues were incubated in serum-free medium, a stimulatory effect of cortisol on tissue phosphatidylcholine synthesis was found in explants from 21-, 24-, 26- and 28-day fetal rabbits; a stimulatory effect of cortisol was observed in 19-day fetal lung explants only if fetal calf serum was present in the culture medium. To assess directly the effect of cortisol on the synthesis of lamellar body phosphatidylcholine, choline incorporation into phosphatidylcholine associated with a purified lamellar body fraction isolated from lung explants of 21- and 28-day fetal rabbits was also investigated. Cortisol caused a marked stimulation of synthesis and accumulation of lamellar body phosphatidylcholine in lung explants from both 21- and 28-day fetal rabbits. The magnitude of the stimulatory effect of cortisol on the rate of synthesis of lamellar body phosphatidylcholine was always greater than the effect of cortisol on the rate of choline incorporation into lipids of tissue homogenates. The relative rates of synthesis of lamellar body phosphatidylinositol and phosphatidylglycerol were also significantly altered in lung explants from 21- and 28-day fetal rabbits by cortisol treatment. Lamellar bodies that were formed initially in the fetal lung explants were enriched in phosphatidylcholine and phosphatidylinositol and had a relatively low phosphatidylglycerol content. With cortisol treatment there was a decrease in the relative rate of synthesis of lamellar body phosphatidylinositol and an increase in the relative rate of synthesis of phosphatidylglycerol. The stimulatory effect of cortisol on the synthesis of lamellar body phosphatidylcholine was observed at an earlier time-point of incubation than was the effect of cortisol on the relative rates of synthesis of lamellar body phosphatidylinositol and phosphatidylglycerol. The temporal sequence of the cortisol-induced changes in the synthesis of lamellar body glycerophospholipids, therefore, reflects that which occurs with maturation in vivo.     

Non-specificity of surfactant deficiency in neonatal respiratory disorders.

The phospholipid content of lung fluid taken from 77 babies during the first day of life was studied. Babies with hyaline membrane disease had low concentrations of the surfactant phospholipids phosphatidylcholine, phosphatidylinositol, and phosphatidylglycerol. The palmitic acid content in phosphatidylcholine was also lower than normal. Surfactant deficiency was not, however, specific for hyaline membrane disease, as similar phospholipid abnormalities were observed in babies with congenital pneumonia and transient tachypnoea of the newborn. These findings have important clinical implications. They are relevant to research into surfactant substitution and cast doubts on the value of the antenatal phospholipid lung profile of amniotic fluid in predicting the risk of hyaline membrane disease.     

Phosphatidylinositol and not phosphatidylglycerol is the important minor phospholipid in rhesus-monkey surfactant

Pulmonary surfactant was isolated from lung tissue and alveolar washes of lungs of adult rhesus monkeys (Macaca mulatta). The phospholipid composition was determined and compared to the composition of human surfactant fractions. Contrary to human surfactant, phosphatidylinositol is the major acidic phospholipid, whereas phosphatidylglycerol is only a minor component in rhesus-monkey surfactant. These differences are not caused by a difference in plasma myo-inositol concentrations between the two species.