Synthesis Of Pulmonary Surfactant Research Articles

Editorial: The granular type II pneumocyte and lung antioxidant defense.

Editorials1 March 1974The Granular Type II Pneumonocyte and Lung Antioxidant DefenseCARROLL E. CROSS, M.D.CARROLL E. CROSS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-3-409 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTwo cell types predominate in mammalian alveolar epithelium: [1] Type I cells (membranous pneumonocytes), which have a small, nucleated cell body with attenuated peripheral cytoplasm containing a relative paucity of intracytoplasmic organelles, and which cover most of the alveolar surface; and [2] Type II cells (granular pneumonocytes), which are nearly cuboidal with abundant cytoplasmic organelles, including moderate amounts of endoplasmic reticulum, ribosomes, and lamellar inclusions, and which cover areas of the alveolar surface not lined by type I cells. The lamellar inclusions of the type II cells represent sites of synthesis of pulmonary surfactant, the phospholipid-rich substance primarily responsible for...

Acute respiratory distress syndrome in pancreatitis.

Analysis of the records of 50 consecutive patients with acute pancreatitis admitted to a general hospital showed that 9 (18%) had diffuse pulmonary infiltrates. Dyspnea and shock were common, and arterial hypoxemia was invariably present in all patients studied (arterial PO2, 44 to 56 mm Hg). Five of the nine patients died with severe hypoxemia despite oxygen therapy. Postmortem studies showed pulmonary congestion and diffuse nonspecific pneumonitis without evidence of bacterial infection. One of the survivors had a gradual improvement in arterial oxygenation over a 4-week period. Pulmonary physiological testing 3 months later showed normal findings, except for a diffusing capacity of 50% of predicted. These findings indicate that severe hypoxemia is common in acute pancreatitis, but with appropriate care the lung disease is largely reversible. Possible pathophysiological mechanisms include injury to the lung by pancreatic enzymes, destruction or impaired synthesis of pulmonary surfactant, and pulmonary congestion secondary to myocardial failure.

Impaired pulmonary surfactant synthesis in starvation and severe nonthoracic sepsis

1. 1. Pulmonary and airway surfactant synthesis and secretion have been compared in fed, starved, and septic rats by analysis of total phospholipid and phosphatidyl choline fractions of extracted lipid. The data are amplified by measurements of rate of incorporation and specific activity of radioactive phosphorus in these fractions. 2. 2. Both starvation and sepsis interfere with synthesis, storage, and secretion of surfactant phospholipids. 3. 3. Evidence suggests that transudation of plasma constituents into the septae and the alveoli during sepsis further inactivates existing surfactant. This is associated with an increase in the frequency of the interstitial pneumonitis characteristic of severe nonthoracic infections. 4. 4. The role of circulating microemboli and peptides originating in the site of infection has been discussed with respect to the initiation of the metabolic and pathologic changes observed. 5. 5. Preservation of surfactant metabolism requires maintenance of nutrition and ventilatory support in addition to surgical management of the septic focus.

De novo fatty acid synthesis and elongation of fatty acids by subcellular fractions of lung

Fatty acid synthesis by subcellular fractions of rabbit lung was studied by measuring the incorporation of either radioactive acetyl coenzyme A or malonyl coenzyme A into long-chain fatty acids. Evidence is presented to support the conclusions that the 95,000 g-supernatant fraction contains the enzymes, i.e., fatty acid synthetase and acetyl coenzyme A carboxylase, necessary for de novo fatty acid synthesis and is capable of synthesizing long-chain fatty acids, probably palmitic acid, under the appropriate conditions. The mitochondrial fraction incorporates the short-chain coenzyme A derivatives into fatty acids predominantly by the elongation pathway. It is suggested that the palmitic acid synthesized in vivo by the de novo fatty acid synthetic pathway, demonstrated in vitro in rabbit lung, may be a source of the lecithin palmitic acid utilized in the synthesis of pulmonary surfactant.

Rates of replacement of lecithins and alveolar instability in rat lungs.

Rates of replacement of lecithins and alveolar instability in rat lungs.

Effect of ventilation on surface forces in excised dogs' lungs.

Effect of ventilation on surface forces in excised dogs' lungs.