6-ketoprostaglandin-f1-alpha and Bronchopulmonary-Dysplasia

6-ketoprostaglandin-f1-alpha has been researched along with Bronchopulmonary-Dysplasia* in 2 studies

Trials

2 trial(s) available for 6-ketoprostaglandin-f1-alpha and Bronchopulmonary-Dysplasia

ArticleYear
Early postnatal dexamethasone therapy may lessen lung inflammation in premature infants with respiratory distress syndrome on mechanical ventilation.
    Pediatric pulmonology, 1997, Volume: 23, Issue:3

    Early postnatal use of dexamethasone has recently been shown to be effective in improving the pulmonary status in premature infants with respiratory distress syndrome (RDS). To study the effect of dexamethasone on pulmonary inflammatory responses, we studied ten infants treated with dexamethasone and ten infants without this treatment. Serial tracheal aspirates were obtained for cell counts, neutrophil counts, total protein concentrations, and leukotriene B4 (LTB4) and 6-keto prostaglandin (PG)F(1 alpha) levels before and after starting the study. Infants in the dexamethasone-treated group required significantly lower mean airway pressures for ventilation and had lower PaCO2 values from day 3 to day 14 than infants in the control group, suggesting better pulmonary function. For infants in the dexamethasone group, the tracheal aspirates showed significantly lower cell and neutrophil counts, protein concentrations, and 6-keto-PGF(1 alpha) and LTB4 levels than in the control group. We conclude that early postnatal dexamethasone therapy may lessen lung inflammation and improve pulmonary function in infants with RDS.

    Topics: 6-Ketoprostaglandin F1 alpha; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Bronchopulmonary Dysplasia; Cell Count; Dexamethasone; Female; Humans; Infant, Newborn; Infant, Premature; Leukotriene B4; Male; Respiration, Artificial; Respiratory Distress Syndrome, Newborn; Time Factors

1997
The silent ductus: its precursors and its aftermath.
    Pediatric cardiology, 1986, Volume: 7, Issue:3

    Prophylactic closure of the patent ductus arteriosus has been recommended as a means of decreasing the morbidity of the very low birth weight neonate. This study was undertaken in order to determine potential risk factors involved in the development of the silent ductus, its impact upon both the early cardiorespiratory symptomatology and the subsequent morbidity of the premature neonate, and finally the potential benefit to be derived from prophylactic closure in this presymptomatic stage. Infants with birth weights of 1000 g or less were studied on days 2-3 of life echocardiographically, clinically, and with determination of plasma dilator prostaglandin levels. On entry to the study, those infants with early evidence of silent left-to-right patent ductus arteriosus (PDA) shunting were randomized to receive either prophylactic indomethacin or placebo therapy. Those infants with no evidence of ductal shunting were not treated at all. Infants with silent PDAs had elevated levels of the dilator prostaglandin metabolite 6-keto PGF1 alpha on admission, although they had no echocardiographic abnormalities. No other risk factors for PDA development could be identified. Silent PDA infants had an increased incidence of subsequent symptomatic PDAs, and overall morbidity and mortality when compared with those with no evidence of PDA (silent or symptomatic). Prophylactic ductal closure decreased the incidence of subsequent PDA development, but had no effect on overall morbidity and/or mortality.

    Topics: 6-Ketoprostaglandin F1 alpha; Bronchopulmonary Dysplasia; Dinoprostone; Ductus Arteriosus, Patent; Humans; Indomethacin; Infant, Low Birth Weight; Infant, Newborn; Prognosis; Prostaglandins E; Risk

1986