Surfactant protein C in fetal and ventilated preterm rabbit lungs. (25/754)

The developing lung contains surfactant protein (SP) C mRNA levels comparable to term values before mature type II cells and alveolar surfactant lipids are detectable. Estimates of the amount of mature SP-C in the alveolar lavages of preterm lungs are not available. We used an antibody to a recombinant human SP-C to measure the amount of SP-C in alveolar lavages of preterm fetal rabbits, ventilated preterm rabbits, and term rabbits. The amounts of SP-C were compared with the amounts of saturated phosphatidylcholine (Sat PC). Median Sat PC amounts increased about 680-fold, and median SP-C values increased by over 5,000-fold in alveolar washes from 27 days gestation to term. There was no increase in Sat PC or SP-C with ventilation at 27 and 28 days gestation, but ventilation increased both Sat PC and SP-C at 29 days gestation. The molar percent of SP-C relative to Sat PC also increased with gestational age and with ventilation at 29 days gestation. proSP-C was abundant in a membrane fraction from lung tissue at 27 and 28 days gestation when minimal mature SP-C was detected in alveolar washes. At 29 days and at term, proSP-C decreased in membrane fractions. The preterm lung that is surfactant lipid deficient is also severely deficient in mature SP-C.  (+info)

SP-B refining of pulmonary surfactant phospholipid films. (26/754)

Pulmonary surfactant stabilizes the alveoli by lining the air-fluid interface with films that reduce surface tension to near 0 mN/m (gamma(min)). Surfactant protein B (SP-B) enhances the surface activity of surfactant phospholipids. A captive bubble tensiometer (CBT) was used to study the properties of adsorbed films of dipalmitoylphosphatidylcholine (DPPC) with acidic 1-palmitoyl-2-oleoyl-sn-glycero-3-[phospho-rac-(1-glycerol)] (POPG) or neutral 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine with (7:3) and without 1% dimeric SP-B. SP-B enhanced the adsorption rate of DPPC-containing neutral or acidic lipid suspensions (1 mg/ml) to a similar extent. Quasi-static cycling of these films revealed that SP-B significantly decreased the film area reduction required to reach gamma(min) for the acidic but not for the neutral system. The results obtained with DPPC-phosphatidylglycerol (PG)-SP-B were consistent with selective DPPC adsorption into the surface monolayer during film formation. Film area reduction required to reach gamma(min) with this system (with and without calcium) approached that of pure DPPC, suggesting selective DPPC insertion and PG squeeze-out. Dynamic cycling of such films showed that larger film area reductions were required to reach gamma(min) for the neutral than for acidic system, even after 20 cycles. Fluorescence microscopy of solvent-spread DPPC-POPG-SP-B planar films revealed highly condensed structures at approximately 25 mN/m, although no specific PG phase-segregated structures could be identified. The study suggests that specific interactions of SP-B with acidic phospholipids of surfactant may be involved in the generation and maintenance of DPPC-rich films in the alveoli.  (+info)

International randomised controlled trial of patient triggered ventilation in neonatal respiratory distress syndrome. (27/754)

AIM: To compare the effects of patient triggered ventilation (PTV) with conventional ventilation (IMV) in preterm infants ventilated for respiratory distress syndrome (RDS). METHODS: Nine hundred and twenty four babies from 22 neonatal intensive care units were assessed. They were under 32 weeks of gestation and had been ventilated for respiratory distress syndrome (RDS) for less than 6 hours within 72 hours of birth. The infants were randomly allocated to receive either PTV or IMV. Analysis was on an "intention to treat" basis. Death before discharge home or oxygen therapy at 36 weeks of gestation; pneumothorax while ventilated; cerebral ultrasound abnormality nearest to 6 weeks; and duration of ventilation in survivors were the main outcome measures. RESULTS: There was no significant difference in outcome between the two groups. Unadjusted rates for death or oxygen dependency at 36 weeks of gestation were 47.4% and 48.7%, for PTV and IMV, respectively; for pneumothorax these were 13.4% and 10.3%; and for cerebral ultrasound abnormality nearest to 6 weeks these were 35.4% and 36.9%. Median duration of ventilation for survivors in both groups was 6 days. Overall, 79% of babies received only their assigned ventilation. PTV babies were more likely to depart from their intended ventilation (27% vs 15%). The trend towards higher pneumothorax rates with PTV occurred only in infants below 28 weeks of gestation (18.8% vs 11.8%). CONCLUSIONS: There was no observed benefit from the use of PTV, with a trend towards a higher rate of pneumothorax under 28 weeks of gestation. Although PTV has a similar outcome to IMV for treatment of RDS in infants of 28 weeks or more gestation, within 72 hours of birth, it was abandoned more often. It cannot be recommended for infants of less than 28 weeks' gestation with the ventilators used in this study.  (+info)

Randomised controlled trial of patient triggered and conventional fast rate ventilation in neonatal respiratory distress syndrome. (28/754)

AIM: To compare patient triggered, with conventional fast rate, ventilation in a randomised controlled trial using the incidence of chronic lung disease as the primary outcome measure. METHODS: Three hundred and eighty six preterm infants with birthweights from 1000 to 2000 g, and requiring ventilation for respiratory distress syndrome within 24 hours of birth, were randomised to receive either conventional or trigger ventilation with the SLE 2000 ventilator. RESULTS: There were no significant differences in the incidence of chronic lung disease (28 day and 36 week definitions), death, pneumothorax, intraventricular haemorrhage, number of ventilator days, or length of oxygen dependency between groups. CONCLUSIONS: Patient triggered ventilation in preterm infants with respiratory distress syndrome is feasible. No significant differences, when compared with conventional fast rate ventilation in important medium and longer term outcome measures, were evident.  (+info)

Randomised controlled trial of postnatal sodium supplementation on oxygen dependency and body weight in 25-30 week gestational age infants. (29/754)

AIM: To compare the effects of early against delayed sodium supplementation on oxygen dependency and body weight, in preterm infants of 25-30 weeks of gestational age. METHODS: Infants were stratified by gender and gestation and randomly assigned to receive a sodium intake of 4 mmol/kg/day starting on either the second day after birth or when weight loss of 6% of birthweight was achieved. Daily sodium intake, serum sodium concentration, total fluid intake, energy intake, clinical risk index for babies (CRIB) score and duration of ventilatory support and additional oxygen therapy were recorded. Infants were weighed daily. Weights at 36 weeks and six months of postmenstrual age were also recorded. RESULTS: Twenty four infants received early, and 22 delayed, sodium supplementation. There were no significant differences in total fluid and energy intake between the two groups. There was a significant difference in oxygen requirement at the end of the first week, with 9% of the early group in air in contrast to 35% of the delayed group (difference 26%, 95% confidence interval 2, 50). At 28 days after birth the proportions were 18% of the early group and 40% of the delayed group (difference 22%, 95% CI -5, 49). Proportional hazards modelling showed early sodium supplementation and lower birthweight to be significantly associated with increased risk of continuing oxygen requirement. The delayed sodium group had a greater maximum weight loss (delayed 16.1%; early 11.4%, p=0.02), but there were no significant differences in time to maximum weight loss, time to regain birthweight, and weight at 36 weeks and 6 months of postmenstrual age. CONCLUSION: In infants below 30 weeks of gestation, delaying sodium supplementation until at least 6% of birthweight is lost has a beneficial effect on the risk of continuing oxygen requirement and does not compromise growth.  (+info)

Reversible adult respiratory distress in primary antiphospholipid syndrome. (30/754)

Antiphospholipid antibody syndrome (APS) is a disorder caused by circulating antibodies reacting with biological membranes and characterized by recurrent thrombosis, chronic thrombocytopenia and miscarriages. It has been reported to occur either as a primary syndrome or secondary to systemic autoimmune disorders. We describe a case of primary APS in a young patient, in whom the clinical course was particularly severe and complicated by a respiratory distress syndrome. The patient was resistant to a number of treatments, and eventually responded to intravenous high dose corticosteroids.  (+info)

Association between the surfactant protein A (SP-A) gene locus and respiratory-distress syndrome in the Finnish population. (31/754)

Respiratory-distress syndrome (RDS) in the newborn is a major cause of neonatal mortality and morbidity. Although prematurity is the most-important risk factor for RDS, the syndrome does not develop in many premature infants. The main cause of RDS is a deficiency of pulmonary surfactant, which consists of phospholipids and specific proteins. The genes underlying susceptibility to RDS are insufficiently known. The candidate-gene approach was used to study the association between the surfactant protein A (SP-A) gene locus and RDS in the genetically homogeneous Finnish population. In the present study, 88 infants with RDS and 88 control infants that were matched for degree of prematurity, prenatal glucocorticoid therapy, and sex were analyzed for SP-A genotypes. We show that certain SP-A1 alleles (6A2 and 6A3) and an SP-A1/SP-A2 haplotype (6A2/1A0) were associated with RDS. The 6A2 allele was overrepresented and the 6A3 allele was underrepresented in infants with RDS. These associations were particularly strong among small premature infants born at gestational age <32 wk. In infants protected from RDS (those that had no RDS, despite extreme prematurity and lack of glucocorticoid therapy), compared with infants that had RDS develop despite having received glucocorticoid therapy, the frequencies of 6A2 (.22 vs.71), 6A3 (.72 vs.17), 6A2/1A0 (.17 vs.68), 6A3/1A1 (.39 vs.10), and 6A3/1A2 (.28 vs.06) in the two groups, respectively, were strikingly different. According to the results of conditional logistic-regression analysis, diseases associated with premature birth did not explain the association between the odds of a particular homozygous SP-A1 genotype (6A2/6A2 and 6A3/6A3) and RDS. In the population evaluated in the present study, SP-B intron 4 variant frequencies were low and had no detectable association with RDS. We conclude that the SP-A gene locus is an important determinant for predisposition to RDS in premature infants.  (+info)

The metabolic effect of antenatal corticosteroid therapy. (32/754)

The use of antenatal dexamethasone to mature the fetal lung in pregnancies likely to deliver before 34 weeks is almost universal. It reduces the incidence of respiratory distress syndrome in the newborn and results in an overall improvement in neonatal morbidity and mortality. Although considered to be generally safe, there are concerns about adverse maternal and fetal effects. In a series of studies, we have found that antenatal dexamethasone administration is associated with reduced placental hormone production and maternal bone formation, impaired glucose tolerance and altered function of the hypothalamic-pituitary-adrenal axis. In this article, we have compared our data with other reports in the human and reviewed the relevant animal data. We conclude that further studies on the long-term effects of antenatal dexamethasone therapy in the human are warranted with particular emphasis on the long-term effects on the fetus.  (+info)