phosphatidyl choline/hypoxia

After acute hypoxia (3 hrs, P-200 mm Hg) content of total phospholipids and of their fractions was not altered in rat lung parenchyma, but the phospholipid composition, changed due to preadministration of hydrocortisone or insulin, was normalized. After the hypoxia concentration of phospholipids in

Changes in the composition and contents of phospholipids and free fatty acids were observed and compared in three groups: (A) unpreconditoned normal controls, (B) exposure to 1 run of hypoxia and (C) exposure to 4 runs of hypoxia. In group B, the content of phosphatidyl ethanolamine (PE),

The phsopholipid composition of lung tissue and lung lavage in rats exposed to acute hypoxia, chronic hypoxia, and acute and chronic hypoxia associated with cold has been estimated and compared with controls. Different fractions of phospholipids were separated by thin layer chromatography. Results

Previous studies demonstrated a protective effect of hypoxia on subsequent death breathing oxygen. Four groups of rats were exposed to air for 120 hours plus 99% O2 for 52 hours (A + O2); 120 hours of hypoxia plus 52 hours 99% O2 (H + O2); 172 hours of only air (A); and 120 hours of only hypoxia

Exposure of adult rats to hypobaric hypoxia caused hypolipidemia, hypotriglyceridemia and hypophospholipidemia. Hypobaric hypoxia produced an increase in liver triglyceride and cholesterol levels and a decrease in lung triglyceride, total phospholipid and phosphatidyl choline. The proportion of

In the presence of ATP, Mg and CoA-SH]1-14C]linoleic acid was incorporated into membrane phospholipids (P2 fraction and synaptosomes) prepared from rat brain cortex. The relative order for linoleate incorporation was: phosphatidyl-choline greater than phosphatidylethanolamine greater than

OBJECTIVE To evaluate the effect of glucocorticoid (GC) in the treatment of septic acute respiratory distress syndrome (ARDS). METHODS ARDS model was reproduced by intraperitoneal injection of E.coli in piglets. Nine male piglets were randomly divided into control (C group), early (GC1) and middle

OBJECTIVE Insulin resistance in diabetes mellitus type 2 (DM2) can result from membrane lipid alterations. Blacks are at a higher risk of developing DM2; therefore, we investigated whether membrane lipid differences exist between blacks and whites and if differences contribute to impaired insulin

Elevations of phospholipid and catecholamine concentrations in the blood are regarded as the vital reactions in asphyxial deaths, which leave few or no morphological signs in the body. These vital reactions were tested here, under strict experimental conditions, employing rapid asphyxia. Rats

Brain microsome phospholipids and their acyl groups, from temperature and oxygen acclimated goldfish, were investigated. At the lower acclimation temperature (5C) the proportion of ethanolamine- to choline-glycerophosphatides (GPE/GPC) was increased, and the proportion of phosphatidal ethanolamine

BACKGROUND Birth asphyxia may result in multiple organ dysfunction such as lung injury. Inhalation of nebulized nitric oxide precursor can selectively reduce pulmonary hypertension. However, it is unknown whether such precursors can alleviate lung injury induced by hypoxia. We evaluated the effect

Moderate hypoxia did not influence the pulmonary incorporation of an intravenous dose of [1-14C]palmitate either in dogs with experimentally produced granulomatous disease or in normal controls. The lung weight in the diseased animals, was, on the average, double that of the controls. There was a

The antihypoxic and antioxidative effects of phosphatidyl choline liposomes have been studied in hypoxic hypoxia, pneumonia, and acute blood loss. It was demonstrated that the body tolerance of persisting hypoxia increased on liposome administration due to elimination of lactate-acidosis, inhibition

On the lining of alveolar membrane of the lung presence of surfactant, a surface tension lowering agent which is a phospholipid in nature, is well established. A good correlation exists between pulmonary lecithin, the principle constituent of surfactant system and alveolar stability. The production