thromboxane-b2 and Respiratory-Distress-Syndrome--Newborn

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

Prostacyclin (PGI(2)) and thromboxane A(2) (TxA(2)) may take part in lung pathology; high concentrations of PGI(2) may protect newborn rabbits against hyperoxic lung injury, and TxA(2) may participate in the development of bronchopulmonary dysplasia (BPD).. To examine in small preterm infants, the relationship between pulmonary PGI(2) and TxA(2) and respiratory distress during the early postnatal period.. The stable metabolite of prostacyclin, 6-keto-prostaglandinF(1 alpha), and that of thromboxane A(2), thromboxane B(2), were quantified by radioimmunoassays in 284 samples of tracheal aspirates from 48 infants (GA: 27.4+/-2.1 week, BW 959+/-334 g) during the first 12 postnatal days.. Mean concentration of 6-keto-prostaglandinF(1 alpha) was 414+/-31 pg/ml (mean+/-S.E.M.), and of thromboxane B(2) was 418+/-37 pg/ml. Correlations existed between 6-keto-prostaglandinF(1 alpha) and gestational age, birth weight, and the initial arterial-alveolar oxygenation ratio. Negative correlations existed between 6-keto-prostaglandinF(1 alpha) and both mean inspiratory oxygen and duration of mechanical ventilation. Indomethacin treatment was associated with lower pulmonary 6-keto-prostaglandinF(1 alpha), but not with lower TxB(2). Thromboxane B(2) correlated positively with gestational age, birth weight, and initial arterial-alveolar oxygenation ratio, and inversely with duration of mechanical ventilation.. In preterm infants, higher pulmonary 6-keto-prostaglandinF(1 alpha) was associated with less severe respiratory distress and with maturity, whereas thromboxane B(2) was associated more strongly with maturity than with respiratory distress.

Topics: 6-Ketoprostaglandin F1 alpha; Epoprostenol; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Intubation, Intratracheal; Lung; Radioimmunoassay; Respiratory Distress Syndrome, Newborn; Thromboxane A2; Thromboxane B2; Trachea

To determine whether number and activation of circulating polymorphonuclear leukocytes (PMNs) and platelets are associated with disease severity in neonatal respiratory distress syndrome (RDS).. Prospective study.. Tertiary neonatal intensive care unit.. Preterm infants with severe (n = 18) or mild to moderate (n = 18) RDS who were consecutively admitted.. PMN and platelet counts and plasma concentrations of elastase-alpha1-proteinase inhibitor (E-alpha1-PI) and thromboxane B2 (TxB2) were recorded each day during the first 5 days of life. E-alpha1-PI-to-PMN and TxB2-to-platelet ratios were calculated to correct for the influence of the PMN and platelet count on elastase and thromboxane release.. From day 2, the severe RDS group had lower median PMN counts (1.5 vs 4.5 x 10/L), lower mean platelet counts (136 vs 230 x 10/L), and more elastase and thromboxane release, indicated by higher median E-alpha1-PI-to-PMN (39.2 vs 13.0 ng/10 PMNs on day 2) and TxB2-to-platelet (2.61 vs 0.52 pg/10 platelets on day 3) ratios than the mild-to-moderate group. Lower PMN and platelet counts and higher elastase and thromboxane release were correlated with birth asphyxia (lower 5-minute Apgar scores and umbilical arterial PH values), higher respiratory requirements (fraction of inspired oxygen and peak inspiratory pressure), and decreased values for continuous measures of RDS severity (ventilatory efficiency index and PaO2-to-alveolar oxygen tension ratio).. Decreased PMN and platelet counts and increased elastase and thromboxane release are correlated with increased RDS severity. Birth asphyxia (hypoxia and acidosis) and tissue injury caused by high-pressure ventilation and hyperoxia may promote this activation process.

Topics: alpha 1-Antitrypsin; Humans; Infant, Newborn; Leukocyte Count; Leukocyte Elastase; Neutrophil Activation; Neutrophils; Platelet Activation; Platelet Count; Prospective Studies; Respiratory Distress Syndrome, Newborn; Severity of Illness Index; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Antithrombin III; Cerebral Hemorrhage; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Prostaglandins; Reference Values; Respiratory Distress Syndrome, Newborn; Thromboxane B2

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

To study the production of proaggregatory thromboxane A2 (TxA2) by fetal and neonatal platelets, blood specimens were collected from umbilical cords immediately after delivery at term (n = 22), from newborn infants during the first 10 days of life (n = 85), from infants between 1 and 3 months of age (n = 14), and from healthy adults (n = 18). The blood samples were allowed to clot spontaneously at +37 degrees C for 60 min, and the concentrations of thromboxane B2 (TxB2), a stable metabolite of TxA2, in the sera were measured by radioimmunoassay and expressed as nanograms of TxB2/10(6) platelets. Platelet TxB2 generation in term infants at the age of 1 day (1.344 +/- 0.253 ng/10(6) platelets, mean +/- SE, n = 9) was higher than that in cord blood (0.634 +/- 0.042 ng/10(6) platelets, n = 22), or in infants of 1-3 months of age (0.881 +/- 0.099 ng/10(6) platelets, n = 14), or in adults (0.869 +/- 0.062 ng/10(6) platelets, n = 18). Increase in TxB2 generation following birth was seen already at the age of 1 h (1.076 +/- 0.114 ng/10(6) platelets, n = 9). TxB2 synthesis in preterm infants (1.032 +/- 0.136 ng/10(6) platelets, n = 10) did not differ from that in term infants on the 1st day of life, and idiopathic respiratory distress syndrome had no effect on it (1.029 +/- 0.079 ng/10(6) platelets, n = 19). Severe birth asphyxia was accompanied by reduced TxB2 formation (0.564 +/- 0.201 ng/10(6) platelets, n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Age Factors; Asphyxia Neonatorum; Blood Platelets; Female; Fetal Blood; Humans; Infant; Infant, Newborn; Male; Respiratory Distress Syndrome, Newborn; Thromboxane B2; Thromboxanes