8-11-14-eicosatrienoic-acid has been researched along with Respiratory-Distress-Syndrome--Newborn* in 2 studies
2 other study(ies) available for 8-11-14-eicosatrienoic-acid and Respiratory-Distress-Syndrome--Newborn
Article | Year |
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Effects of early nutrition on free radical formation in VLBW infants with respiratory distress.
We studied the development of essential fatty acid deficiency (EFAD) and its effects together with those of vitamin E deficiency on the free radical formation of very low birth weight (VLBW) infants with respiratory distress.. Infants were divided into three groups based on the way each was supplied with daily total energy intake: (1) by fat free parenteral nutrition only or by nutrition composed of (2) less than or (3) higher than 25% of total daily energy intake given in oral feeding. We measured plasma lipid parameters and autoxidative susceptibility (AOS) of red blood cells (RBCs).. Plasma concentrations of linoleic acid were low in all the groups. After at least 14 days of feeding, eicosatrienoic acid (EA) was not detected. One week after the introduction of oral feeding, the abnormal triene/tetraene ratio of the groups had decreased, but was not normalized. Vitamin E deficiency was associated with significantly increased AOS, but EFAD was not. The two factors together caused an increase of AOS, that was additive.. Our data confirm that EFAD increases AOS of RBCs in VLBW infants. We assume that prevention of EFAD in VLBW infants could decrease the prevalence of complications associated with free radical formation. Topics: 8,11,14-Eicosatrienoic Acid; Aging; Dietary Fats; Energy Intake; Enteral Nutrition; Fatty Acids, Essential; Free Radicals; Humans; Infant Nutritional Physiological Phenomena; Infant, Newborn; Infant, Very Low Birth Weight; Linoleic Acid; Lipids; Parenteral Nutrition; Respiratory Distress Syndrome, Newborn; Thiobarbituric Acid Reactive Substances; Vitamin E; Vitamin E Deficiency | 2000 |
Essential fatty acids, prostaglandins, and respiratory distress syndrome of the newborn.
The lungs are a major metabolic site for the synthesis, release, and degradation of prostaglandins. Prostaglandins of the E and F series exert a potent physiological effect on the smooth muscle of blood vessels and the tracheobronchial tree; prostaglandin E dilates while prostaglandin F constricts. Thus, altered prostaglandin metabolism may contribute to the pathophysiology of respiratory distress syndrome (RDS). Twenty-one infants with RDS and ten age- and weight-matched controls were studied by analyzing their plasma for prostaglandins and their precursor essential fatty acids. The two groups showed no differences in the essential fatty acid prostaglandin precursors, dihomo-gamma-linolenic and arachidonic acids. During the acute phase of RDS, plasma levels of the primary prostaglandins E and F are significantly elevated compared with control values and the ratio of prostaglandin E to prostaglandin F significantly reduced. Prostaglandins E and F returned to control values on recovery from the acute stage of the disease. Two infants with persistent patent ductus arteriosus had significantly elevated prostglandin E values in their plasma compared with controls. The elevated levels of circulating plasma prostaglandins E and F and the reversal of their ratio during the acute phase of RDS may have adverse pulmonary and multisystem effects. Topics: 8,11,14-Eicosatrienoic Acid; Arachidonic Acids; Cholesterol Esters; Fatty Acids, Essential; Humans; Infant, Newborn; Lung; Phospholipids; Prostaglandins; Prostaglandins E; Prostaglandins F; Respiratory Distress Syndrome, Newborn | 1978 |