Phosphatidylcholine metabolism of rat trachea in relation to lung parenchyma and surfactant

Abstract

Pulmonary surfactant prevents alveolar collapse and contributes to airway patency by reducing surface tension. Although alveolar surfactant, consisting mainly of phospholipids (PL) together with neutral lipids and surfactant-specific proteins, originates from type II pneumocytes, the contribution of airway epithelia to the PL fraction of conductive airway surfactant is still debated. We, therefore, analyzed the composition, synthesis, and release of phosphatidylcholine (PC) molecular species as the main surfactant PL of the rat trachea compared with the lung. Analyses of individual PC molecular species with HPLC and electrospray ionization mass spectrometry revealed that the rat trachea contained and synthesized much more palmitoyloleoyl-PC, palmitoyllinoleoyl-PC, and palmitoylarachidonoyl-PC, together with increased amounts of alkylacyl-PC, and less surfactant-specific species such as dipalmitoyl-PC than the lung. Organ cultures with [methyl-3H]choline as precursor of PC revealed that, in the trachea, synthesized PC was retained in the tissue, rather than secreted. [Methyl-3H]choline-labeled dipalmitoyl-PC was a negligible component in the trachea, and, in contrast to the lungs, palmitoyloleoyl-PC was enriched in tracheal secretions. We conclude that the surfactant fraction in the airways does not originate from the airways but is produced in the alveolar space and transported upward.

Tensiometric and Phase Domain Behavior of Lung Surfactant on Mucus-like Viscoelastic Hydrogels

“…The composition of CAS is closely represented by pulmonary surfactant generated from Type II cells in the alveoli 22–23 . From the alveolar spaces, pulmonary surfactant is carried up the airways due to the surface tension gradient and the mucociliary escalator 22, 24 . Local production and release of phospholipids by tracheal epithelial cells 25–26 and the submucosal glands of both human tracheal and bronchial biopsy specimens 27 have also been detected, thus both sources likely contribute to airway surfactant composition.…”

Molecular and functional changes of pulmonary surfactant in response to hyperoxia

“…Metabolism of individual PC molecular species was investigated by using isolated perfused rat lungs as described before. 29 After anaesthesia the trachea was cannulated and lung ventilation started using a Harvard rodent ventilator (model 683, Harvard apparatus, South Nattick, MA). After opening the thorax the pulmonary artery was cannulated and perfusion started.…”

“…For perfusion a Krebs-Ringer bicarbonate solution (378C, pH 7.35-7.40) was used, which was supplemented with 5% bovine serum albumin (fraction V, >96% purity, Sigma, Steinheim, Germany), 5.6 mmol/L glucose, 2 mmol/L glycerol, 1 mmol/L sodium acetate, 0.1 mmol/L sodium palmitate, and 0.1 mmol/L sodium oleate as previously described. 29 The medium was recycled from a reservoir through a 378C tempered aerator for equilibration with a water saturated gas mixture of 95% oxygen/5% carbon dioxide. Isolated lungs were perfused via hydrostatic pressure of 13-15 cm H 2 O, which resulted in perfusion rates of 7-8 ml/min.…”

Surfactant-Associated Protein B Kinetics In Vivo in Newborn Infants by Stable Isotopes

“…Because Clara cells from the conductive airways are able to synthesize SPs (21,22), further studies will be needed to ascertain differences between surfactant samples from TA and alveolar surfactant. Several investigators found similar surfactant composition in TA and bronchoalveolar lavage fluid (23,24), but SP-A, SP-B, and SP-C were found to be lower in TA than in lung lavage fluid (23). Of note, surfactant analysis from TA is currently the standard method for the study on surfactant in human research (3).…”