thromboxane-b2 has been researched along with Infant--Premature--Diseases* in 7 studies
2 trial(s) available for thromboxane-b2 and Infant--Premature--Diseases
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Decreased lipid intake reduces morbidity in sick premature neonates.
For an investigation of the clinical sequelae of parenteral lipid infusions during the first week of life, 42 neonates (less than 1750 gm birth weight) were randomly assigned to receive parenteral alimentation with (IL) (Vitrum) or without a parenteral lipid infusion (NL) for 5 days. Follow-up clinical status was monitored and compared, and plasma prostaglandin levels were analyzed. Chronic lung disease was increased in duration and tended to be more severe after lipid administration. The number of days of mechanical ventilation (37 +/- 35 vs 21 +/- 18) and supplemental oxygen therapy (51 +/- 39 vs 28 +/- 23) was significantly increased in the IL group. Five IL infants developed stage 3 bronchopulmonary dysplasia, in comparison with none of the NL infants. Seven IL infants were discharged on a regimen of supplemental oxygen therapy versus none of the NL infants. Thromboxane B2 levels were significantly increased in the babies receiving Vitrum. We conclude that early administration of Vitrum in the premature neonate is associated with increased respiratory difficulty in the ensuing weeks of life. Topics: 6-Ketoprostaglandin F1 alpha; Clinical Trials as Topic; Double-Blind Method; Fat Emulsions, Intravenous; Hemodynamics; Humans; Infant, Newborn; Infant, Premature, Diseases; Oxygen; Parenteral Nutrition, Total; Prognosis; Prostaglandins; Random Allocation; Thromboxane B2 | 1988 |
Randomized indomethacin trial for prevention of intraventricular hemorrhage in very low birth weight infants.
We admitted 48 preterm neonates (600 to 1250 gm birth weight, normal 6-hour echoencephalograms) to a randomized prospective indomethacin or placebo trial for the prevention of neonatal intraventricular hemorrhage. Beginning at 6 postnatal hours, indomethacin or placebo was administered intravenously every 12 hours for a total of five doses. Cardiac ultrasound studies to assess the status of the ductus arteriosus were performed at 6 postnatal hours and on day 5. Urinary output, serum electrolytes, and renal and clotting functions were monitored. No differences in birth weight, gestational age, Apgar scores, or ventilatory needs were noted between the two groups. Six infants given indomethacin had intraventricular hemorrhage, compared to 14 control infants (P = 0.02). The indomethacin-treated group had significant decreases in serum prostaglandin values 30 hours after the initiation of therapy. The overall incidence of patent ductus arteriosus was 82% at 6 postnatal hours; 84% of the indomethacin-treated infants experienced closure of the ductus, compared to 60% of the placebo-treated patients. Closure of the ductus was not related to incidence of intraventricular hemorrhage. We speculate that indomethacin may provide some protection against neonatal intraventricular hemorrhage by acting on the cerebral microvasculature. Topics: 6-Ketoprostaglandin F1 alpha; Cerebral Hemorrhage; Clinical Trials as Topic; Ductus Arteriosus, Patent; Echocardiography; Humans; Indomethacin; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature, Diseases; Prospective Studies; Random Allocation; Thromboxane B2 | 1985 |
5 other study(ies) available for thromboxane-b2 and Infant--Premature--Diseases
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Chorioamnionitis and ontogeny of circulating prostaglandin and thromboxane in preterm infants.
Our objective was to determine the effect of chorioamnionitis on plasma prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) during the first week in preterm infants. Plasma PGE2 and TxB2 were measured at 1, 3, and 7 days of age in preterm infants (birth weights 501 to 1500 g), with ( N = 26) and without ( N = 22) chorioamnionitis. Infants with maternal chorioamnionitis had significantly lower mean gestational age ( P = 0.0001) and birth weight ( P = 0.03) and a marginally higher rate of bronchopulmonary dysplasia (37% versus 12.5, P = 0.05), a result that may be related to the lower mean gestational age. Plasma PGE2 and TxB2 varied widely, more so on the first day but did not significantly differ between the two groups. TxB2 was lower among infants who died or developed morbidities. Circulating PGE2 and TxB2 concentrations in preterm infants in the first week vary considerably, are relatively unaltered by chorioamnionitis, and are lower in association with mortality and clinical morbidities. Further research on their role in the causation of adverse neonatal outcomes is necessary. Topics: Adolescent; Adult; Anti-Inflammatory Agents, Non-Steroidal; Birth Weight; Bronchopulmonary Dysplasia; Chorioamnionitis; Dinoprostone; Female; Gestational Age; Humans; Indomethacin; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Pregnancy; Pregnancy Outcome; Respiratory Distress Syndrome, Newborn; Thromboxane B2; Young Adult | 2008 |
Possible platelet contribution to pathogenesis of transient neonatal hyperammonaemia syndrome.
The pathogenesis of the transient neonatal hyperammonaemia syndrome is largely unknown. The role of platelet activation was investigated in three preterm infants with this syndrome by non-invasive methods. In all three infants, urinary concentrations of beta-thromboglobulin and 11-dehydrothromboxane B2 levels were much higher during the hyperammonaemia than those in ten control preterm infants. It is possible that transient platelet activation occurs in the portal system of these infants, thereby causing the hyperammonaemia. Topics: Ammonia; beta-Thromboglobulin; Catheterization; Evaluation Studies as Topic; Female; Humans; Infant, Newborn; Infant, Premature, Diseases; Male; Metabolic Diseases; Platelet Activation; Syndrome; Thromboxane B2; Time Factors | 1991 |
Eicosanoid levels in CSF of premature infants with posthemorrhagic hydrocephalus.
The cerebrospinal fluid (CSF) of 11 premature infants suffering from posthemorrhagic hydrocephalus was examined by radioimmunoassay for prostaglandin (PG) E2, PGF2 alpha, PGD2, 6-keto PGF1 alpha, thromboxane B2 (TxB2) and peptidoleukotrienes (LTC4/LTD4). The LTs were detected in the CSF of more of these patients (70%) than any of the other eicosanoids, and usually in the highest concentration. Among the 11 posthemorrhagic patients CSF eicosanoid levels were highest when determined soon after injury. Moreover, the variety of eicosanoids present, as well as concentrations, in these infants decreased with time. The types of eicosanoids most evident in the CSF of patients who required shunting were TxB2 and LTs, being present together in 5 of 6 (83%) of these infants. In contrast, 1 of 5 (20%) of the patients who did not require this neurosurgical intervention contained both TxB2 and LTs, the remaining having only one or neither eicosanoid. The highest average concentration for each eicosanoid studied was (pg/ml): PGE2, 628; PGF2 alpha, 985; PGD2, 1410; 6-keto PGF1 alpha, 544; TxB2, 486 and LTs, 1229. This study is the first to demonstrate that the CSF of preterm infants may contain a wide variety of eicosanoids and indicates that these lipids are a manifestation of neurological assault. Topics: 6-Ketoprostaglandin F1 alpha; Cerebral Hemorrhage; Dinoprost; Dinoprostone; Eicosanoids; Humans; Hydrocephalus; Infant, Newborn; Infant, Premature, Diseases; Leukotrienes; Prostaglandin D2; Thromboxane B2 | 1990 |
Systemic production of prostacyclin and thromboxane A2 does not correlate with patency of the ductus arteriosus in very low birth weight infants.
Urinary excretion of prostacyclin and thromboxane metabolites (2,3-dinor-6-ketoprostaglandin F1 alpha, thromboxane B2, and 2,3-dinor-thromboxane B2) as indices of systemic biosynthesis was prospectively determined in nine premature infants during the first 10 days of life, by gas chromatography-mass spectrometry. The patients ranged in gestational age from 27 to 29 weeks and in birth weight from 720 to 980 gm. Four infants developed symptomatic patent ductus arteriosus (PDA). Excretion of all metabolites exceeded adult values on the basis of body surface area at birth, reached a maximum on the fourth day of life, was related to urine output, and did not distinguish patients with and without symptomatic PDA. We conclude that neither circulating prostacyclin nor thromboxane A2 contribute significantly to the pathophysiology of symptomatic PDA in very low birth weight infants. Topics: 6-Ketoprostaglandin F1 alpha; Ductus Arteriosus, Patent; Epoprostenol; Gas Chromatography-Mass Spectrometry; Gestational Age; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature, Diseases; Prospective Studies; Thromboxane B2 | 1986 |
Plasma 6-keto prostaglandin F1 alpha and thromboxane B2 in sick preterm neonates.
To determine if vascular abnormalities in preterm neonates might be related to vasoactive prostaglandins, stable prostacyclin (6-KPGF1 alpha) and thromboxane A2 (T X B2) metabolites in arterial blood were measured at less than or equal to 6 hours after birth and at 24, 48, and 72 hours using a radioimmunoassay. Neonates of less than 32 weeks gestation (N = 26) were diagnosed as having either the idiopathic respiratory distress syndrome (IRDS, N = 15) or pulmonary edema (PE, N = 11), and were also grouped according to the presence or absence of intracranial hemorrhage (ICH, N = 11) or patent ductus arteriosus (PDA, N = 10). Initial plasma 6-KPGF1 alpha was greater in neonates with ICH (0.23 +/- 0.04 ng/ml, mean +/- SE) than without ICH (0.11 +/- 0.04, p less than 0.05). Neonates with both ICH and IRDS (N = 8) had significantly elevated T X B2 at all sampling times compared to neonates with IRDS and no ICH (N = 7). Both T X B2 and 6-KPGF1 alpha increased with time in those with major ICH. Among neonates without ICH, 7 with IRDS had higher initial 6-KPGF1 alpha (0.19 +/- 0.07 ng/ml) and lower T X B2 (0.15 +/- 0.04 ng/ml) than 8 with PE (0.04 +/- 0.01 and 0.37 +/- 0.09 ng/ml, respectively). The initial 6-KPGF1 alpha (0.024 + 0.003 ng/ml), measured in neonates with PE and without PDA or ICH (N = 6), was significantly less than the corresponding value in the other neonates (0.201 +/- 0.036 ng/ml) (N = 20). Topics: 6-Ketoprostaglandin F1 alpha; Cerebral Hemorrhage; Ductus Arteriosus, Patent; Humans; Infant, Newborn; Infant, Premature, Diseases; Pulmonary Edema; Respiratory Distress Syndrome, Newborn; Thromboxane B2; Thromboxanes | 1985 |