Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

Hallman, Mikko; Enhörning, Göran; Possmayer, Fred

doi:10.1203/00006450-198503000-00006

Cited by 78 publications

(25 citation statements)

References 19 publications

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“…This is in accordance with previous studies indicating a relative amount of 16 In the current investigation, PI presented a FA profile nearly equal to that of PG, which is not surprising in view of the common synthesis pathway of these two PLs, whereby both originate from the same precursor, cytidine diphosphodiacylglycerol (CDP-DAG) (18). This observation further supports the assumption that the acidic PI may fully replace PG during the neonatal development period (19), as also suggested by in vitro studies addressing the biophysical activity of PG-enriched versus PI-enriched PL mixtures (20,21). Finally, the PG and PI FA compositions are in contrast to the composition of membrane-associated PI which possesses a high percentage of arachidonic acid ‫ف(‬ 30%) and low amounts of oleic acid ‫ف(‬ 7%) (22,23).…”

Section: Discussionsupporting

confidence: 75%

Alteration of Fatty Acid Profiles in Different Pulmonary Surfactant Phospholipids in Acute Respiratory Distress Syndrome and Severe Pneumonia

Schmidt

Meier

Yabut-Perez

et al. 2001

Am J Respir Crit Care Med

118

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Impairment of alveolar surfactant function has been documented in the acute respiratory distress syndrome (ARDS) and in severe pneumonia (PNEU); however, the underlying mechanisms are not completely understood. In the current report we present a detailed analysis of fatty acid (FA) profiles of different surfactant phospholipid (PL) classes isolated from bronchoalveolar lavage fluids (BALF) and large surfactant aggregates (LSA) from mechanically ventilated patients with ARDS (n = 8), ARDS associated with lung infection (ARDS + PNEU, n = 9), and PNEU (n = 22). Healthy volunteers served as control subjects (n = 8). PLs were isolated by thin-layer chromatography, and the FA profile of each PL class was assessed by gas chromatography. In addition, the minimal surface tension (gamma min) of untreated LSA and of LSA after supplementation with additional dipalmitoylated phosphatidylcholine (DPPC) was analyzed (pulsating bubble surfactometer). As compared with control LSA, the percentage of palmitic acid in phosphatidylcholine (PC) was significantly decreased in all patient groups (ARDS 63.0 +/- 2.0%, ARDS + PNEU 64.6 +/- 4.9%, PNEU 65.6 +/- 1.5%, control subjects 80.1 +/- 1.7%), whereas the relative amount of unsaturated species in PC increased significantly in all groups. Phosphatidylglycerol (PG) and phosphatidylinositol (PI) presented similar FA profiles in control subjects, but differed in the patients. The FA pattern of sphingomyelin (SPH) and phosphatidylethanolamine (PE) displayed only minor changes under conditions of respiratory failure. As compared with control subjects a highly significant increase of gamma min from near zero to approximately 16 mN/m was observed in all patients and was found to be inversely correlated to the percentage of palmitic acid in PC of LSA or BALF. Accordingly, values for gamma min were significantly improved upon secondary supplementation of LSA with DPPC up to control values. We conclude that marked changes in the FA composition of the predominant surfactant PL classes occur, both in ARDS triggered by nonpulmonary events and PNEU. The marked reduction of palmitic acid in the PC fraction may be related to changes in surfactant function under these conditions.

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Section: Discussionsupporting

confidence: 75%

Alteration of Fatty Acid Profiles in Different Pulmonary Surfactant Phospholipids in Acute Respiratory Distress Syndrome and Severe Pneumonia

Schmidt

Meier

Yabut-Perez

et al. 2001

Am J Respir Crit Care Med

118

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“…Animals fed myoinositol rather than glucose have a marked reduction in surfactant PG and an increase in PI (22) yet PG-deficient surfactant functions normally (22,23). At the gestational age of the animals in this study, high fetal levels of inositol may have blocked phosphatidyltransferase, the enzyme responsible for PG synthesis; this possibility is supported by evidence that fetal rhesus monkeys do not normally synthesize PG before 155 days' gestation (24).…”

Section: Discussionsupporting

confidence: 68%

Surfactant Quantity and Composition during Recovery from Hyaline Membrane Disease

et al. 1986

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ABSTRACT. The appearance of phosphatidylglycerol in TLC, total lung capacity (in vivo) the tracheal wash of infants with hyaline membrane disease V,,,, maximal lung volume (postmortem) (HMD) has been reported to be associated with clinical ANOVA, one-way analysis of variance signs of recovery. We analyzed lung tissue and bronchoalveolar lavage surfactant in an animal model of HMD to determine whether phosphatidylglycerol or some other component is necessary -for ricGkry. The amount and composition of phospholipid (PL) was determined in the premature Macaca nemestrina monkey (140 days' gestation) during an acute stage of HMD, and in two stages of recovery. These changes were compared to observations made in healthy premature controls (140 days), gestational age-matched fetuses (140 days), and fetuses of 150 days' gestation (term = 168 days). The amount of PL and its surfactant composition in lung homogenates of the right lower lobe and in lavage of the excised left lung was determined. Compared to 140-day fetuses, the healthy controls had a several-fold increase in lavage PL and disaturated phosphatidylcholine (DSPC) during the first few days of life (p < 0.05). Prior to recovery, animals with HMD had no such increase in lavage PL or DSPC and demonstrated poor deflation stability. Recovery was associated with increased tissue and lavage PL ( p < 0.05) and increased fractions of phosphatidylinositol and DSPC ( p < 0.05), but not phosphatidylglycerol. The tissue compositional changes observed during recovery reflected maturational changes observed in the fetal animals studied at 10 days' greater gestational age. Increases in lavage DSPC beyond 2 mg/g dry lung were not associated with further increases in deflation stability. We conclude that increases in DSPC and phosphatidylinositol are associated with recovery from HMD but phosphatidylglycerol does not appear necessary for either improved deflation stability or clinical recovery. (Pediatr Res 20: 1243-1247, 1986 Abbreviations HMD, hyaline membrane disease PL, phospholipid PC, phosphatidylcholine DSPC, disaturated phosphatidylcholine UPC, unsaturated phosphatidylcholine PG, phosphatidylglycerol PI, phosphatidylinositol PE, phosphatidylethanolamine PS, phosphatidylserine SPH, sphingomyelin Received March 20, 1986; accepted July 11, 1986 It is not known whether or not recovery from HMD is contingent on the production of a minimal amount of surface active material and, if so, how much is needed. Although it has been proposed that certain surfactant components, such as PG, may be necessary for recovery (I), studies on pulmonary surfactant composition in human infants during recovery have been limited to examination of tracheal wash. Because of the low mortality during recovery from HMD, it has been impossible to determine the changes in tissue production of PL during recovery or to relate these changes to PL present in the alveolar lavage. The appropriate balance of tissue and alveolar quantities, and the optimal composition of surfactant components needed for recover...

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“…35 Furthermore, PC and not PG has been shown to be the critical phospholipid with sufficiently low surface tensile properties to maintain surface activity and airway patency, 41,42 and in earlier studies, diet-induced surfactant PG deficiency had no deleterious effects on surfactant activity. 43 Our results support the specificity of action of the added lipolytic enzymes as opposed to nonspecific perturbation of surfactant function by excess protein, because the BSA in the reaction buffer and control did not cause surfactant dysfunction in CS assays. However, other eosinophil proteins may have the capacity to contribute to surfactant dysfunction.…”

Section: Discussionsupporting

confidence: 83%

Combined activities of secretory phospholipases and eosinophil lysophospholipases induce pulmonary surfactant dysfunction by phospholipid hydrolysis

Kwatia

Doyle

Cho

et al. 2007

Journal of Allergy and Clinical Immunology

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Composition and Surface Activity of Normal and Phosphatidylglycerol-Deficient Lung Surfactant

Cited by 78 publications

References 19 publications

Alteration of Fatty Acid Profiles in Different Pulmonary Surfactant Phospholipids in Acute Respiratory Distress Syndrome and Severe Pneumonia

Alteration of Fatty Acid Profiles in Different Pulmonary Surfactant Phospholipids in Acute Respiratory Distress Syndrome and Severe Pneumonia

Surfactant Quantity and Composition during Recovery from Hyaline Membrane Disease

Combined activities of secretory phospholipases and eosinophil lysophospholipases induce pulmonary surfactant dysfunction by phospholipid hydrolysis

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