Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchopulmonary dysplasia (BPD) is a significant cause of chronic pulmonary disease following mechanical ventilation of newborn infants. Although the exact pathogenesis of BPD has yet to be elucidated, high concentration of supplemental oxygen delivered by positive pressure through an endotracheal tube is thought to be a major predisposing factor. The only reported clinical trial of the administration of an exogenous antioxidant as vitamin E (20 mg/kg/day I.M.) to premature infants with respiratory distress syndrome who were receiving supplemental oxygen greater than 40% showed a shorter exposure to all levels of supplemental oxygen when compared to a control group. No roentgenographic changes of BPD were noted in any vitamin-E-treated infants. Vitamin E may modify the development of BPD, but until further clinical trials demonstrate a significant reduction in the incidence and severity of BPD, efforts should be made to minimize exposure to any of the associated factors in the pathogenesis of BPD.
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PMID:A possible role of vitamin E in the prevention or amelioration of bronchopulmonary dysplasia. 54 12

This study was undertaken to test chronic feeding of some normal dietary constituents on susceptibility to oxygen toxicity. Eight-week-old male CD-1 mice were fed a semi-purified diet simulating that of the average American male and supplemented with either vitamin E, vitamin K3, selenium, or the sulfur amino acids methionine and cystine. After 2, 4, 8, or 16 weeks, groups of mice were exposed to oxygen at 1, 4, or 8 ATA and times to respiratory distress, convulsion, and death recorded. Vitamin E and amino acid supplementation had no effect whereas vitamin K and selenium supplements increased time to death at 1 ATA. Only the effect of selenium was statistically significant. All diets significantly increased the time of onset of the measured parameters beginning after 4 weeks, suggesting that one or more constituents of the basal diet afforded some protection against oxygen toxicity.
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PMID:Effect of dietary "antioxidant" supplementation on the susceptibility to oxygen toxicity in mice. 125 6

Plasma vitamin E levels were determined serially in preterm infants surviving respiratory distress syndrome (RDS) and in premature infants without RDS (control). Vitamin E intakes of the RDS and control infant group were not significantly different. The results of the study show that preterm infants surviving RDS have a persistent low plasma vitamin E level throughout the first 8 weeks of life. In contrast, in premature infants without RDS the plasma vitamin E level gradually increases to the adult level throughout the first 8 weeks of life. It is concluded that data on plasma vitamin E levels in premature infants with and without RDS should not be pooled together to obtain reference values. It is further suggested that premature infants with RDS might need more supplemental vitamin E than premature infants without RDS.
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PMID:Persistent low plasma vitamin E levels in premature infants surviving respiratory distress syndrome. 376 70

Chemoattractants such as N-formylmethionyl leucyl phenylalanine (FMLP) cause neutropenia in vivo. The sequestered neutrophils may block the microvasculature and contribute to respiratory distress. Neutrophils from humans receiving 1600 units vitamin E per day have reduced oxidative activity. To test whether vitamin E attenuates the responses of neutrophils to FMLP in vivo we gave rabbits four daily intramuscular injections of 100 mg vitamin E. Serum levels of the vitamin were 2.34 +/- 0.15 mg% compared to 0.19 +/- 0.04 mg% in control rabbits receiving placebo injections. On the fifth day testing was done before and after injecting FMLP. Variables monitored were the absolute granulocyte count (AGC), systolic, diastolic and mean blood pressures (MBP), heart rate, PO2, PCO2, pH and respiratory rate. When 0.5 microgram FMLP was injected intravenously the AGC decreased (at 2.5 min the percentage change was -89.7 +/- 8.0 with vitamin E and -97.0 +/- 2.7 without vitamin E; P = 0.2). MBP decreased also (% change, -29.0 +/- 13.0 with vitamin E and -36.3 +/- 16.0, without vitamin E). By 15 min recovery was seen (AGC % change, -26.0 +/- 17 with vitamin E and -78.7 +/- 10.5, without vitamin E; P = 0.01; MBP % change, -9.3 +/- 3.8 with vitamin E and -52.3 +/- 10.1 without vitamin E). Chromatographic analysis of serum extracts revealed increases in 6-keto-PGF1 alpha after stimulation. Studies with [3h]thymidine-labelled neutrophils showed that the sequestered cells return to the circulation. Vitamin E might facilitate this return by altering the adherence of neutrophils to endothelium. This possibility was tested by measuring the adherence to cultivated rabbit aorta endothelial monolayers of FMLP-stimulated neutrophils from vitamin E-treated rabbits. The percentage of neutrophils adhering was 32.5 +/- 3.5 with vitamin E and 60.0 +/- 7.1, without vitamin E. Thus vitamin E promotes the return of neutrophils to the circulation after chemotactic challenge and may do so by reducing their adherence to endothelium.
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PMID:The effect of vitamin E on rabbit neutrophil activation. 655 3

The effect of vitamin E administered during the acute phase of therapy for respiratory distress syndrome (RDS) on the development of retinopathy of prematurity (ROP) was evaluated in a randomized double-masked study. One hundred neonates received either vitamin E or placebo intramuscularly within the first 24 hours of birth and at 24, 48, and 168 hours respectively. Additional doses were given twice weekly while the infant remained in an oxygen-enriched environment and could not tolerate feedings and vitamin supplements. Parenteral vitamin E-treated infants had significantly increased serum vitamin E levels compared to placebo-treated infants. Most placebo-treated patients attained normal serum vitamin E levels during the second week of life because of nutritional sources of vitamin E. Infants in both groups had RDS of similar severity. Seventy-four infants, 37 vitamin E-treated and 37 placebo-treated, survived longer than 10 days and had ophthalmologic examinations. Active changes of Stage I and Stage II ROP were noted in 17 of those patients; 9 (24.3%) vitamin E-treated and 8 (21.6%) placebo-treated patients (P = 0.572). No infants developed severe cicatricial changes, and their retinal findings regressed. The incidence of risk factors associated with ROP development occurred equally in the vitamin E-treated and placebo-treated infants that developed ROP. Thus, vitamin E-administration as described in this study did not result in any further reduction in the incidence of the active stages of ROP over that seen with standard neonatal care, which included daily oral Vitamin E supplements.
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PMID:Influence on retrolental fibroplasia of intramuscular vitamin E administration during respiratory distress syndrome. 704 Oct 39

Premature infants have a lower selenium concentration in serum than full-term infants and children. The selenium concentration goes down quickly in infants treated for respiratory distress syndrome without supplementation. One premature infant with bronchopulmonary dysplasia had persistently low concentrations of selenium. Vitamin E supplements did not affect the serum selenium concentration in healthy premature infants. Supplementation with 3 microgram/kg of selenium in parenteral fluids prevented the fall in the concentration seen in other infants not supplemented. Premature infants and especially those treated with oxygen may warrant selenium supplementation to the parenteral nutrition solution. Vitamin E supplements alone are apparently not sufficient to prevent selenium deficiency and potential oxygen toxicity.
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PMID:Selenium in premature infants. 719 73

The recent identification of Vitamin E acetate as one of the causal agents for the e-cigarette, or vaping, product use associated lung injury (EVALI) is a major milestone. In membrane biophysics, Vitamin E is a linactant and a potent modulator of lateral phase separation that effectively reduces the line tension at the two-dimensional phase boundaries and thereby exponentially increases the surface viscosity of the pulmonary surfactant. Disrupted dynamics of respiratory compression-expansion cycling may result in an extensive hypoxemia, leading to an acute respiratory distress entailing the formation of intraalveolar lipid-laden macrophages. Supplementation of pulmonary surfactants which retain moderate level of cholesterol and controlled hypothermia for patients are recommended when the hypothesis that the line-active property of the vitamin derivative drives the pathogenesis of EVALI holds.
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PMID:Vitamin E acetate as linactant in the pathophysiology of EVALI. 3325 4