Eight-epi-PGF2alpha: a possible marker of lipid peroxidation in term infants with severe pulmonary disease.

A prostaglandin F2-like compound, 8-epi-PGF2alpha, formed from oxidation of arachidonate, has been proposed as an indicator of lipid peroxidation. We determined whether tracheal aspirate or urinary 8-epi-PGF2alpha levels would differ over time or between infants in a control group and infants with severe respiratory failure. We correlated tracheal aspirate 8-epi-PGF2alpha levels with the fraction of inspired oxygen and with mean airway pressures at 24 and 48 hours of life. Levels in tracheal aspirates were in the range of 0 to 36 pg/microg of fSC of IgA and were higher in infants with severe pulmonary disorders compared with those in infants in the control group (p < 0.02). Urinary concentrations did not discriminate between sick infants and infants in the control group.

Diuresis and respiratory distress syndrome: physiologic mechanisms and therapeutic implications.

Previous studies have suggested that spontaneous diuresis may be important to the recovery from respiratory distress syndrome in preterm infants. Daily quantification of fluid intake (1) and urine output (O) were recorded, and O/I and alveolar-arterial oxygen gradients (AaDO2) were determined for sequential eight-hour periods in 10 inborn premature infants with RDS. Sequential timed-urine-plasma collections were obtained during the first four days of life to evaluate the role of hormonal and vasoactive factors in the acute phase of RDS. Diuresis (O/I greater than 0.80) occurred at 25 to 32 hours, preceded any significant improvement in AaDO2 (which occurred at 57 to 64 hours), and was associated with a 6.2 +/- 1.4% decrease in body weight. Although there was no significant change in glomerular filtration rate, plasma AVP concentrations, or urinary excretion of AVP in the infants, there were significant decreases in both plasma concentrations and urinary excretion of 6-keto-PGF1 alpha (stable metabolite of prostacyclin) in sequential studies. These results suggest that changes in renal function or AVP may not be of primary importance in the diuresis associated with RDS, and that decreasing levels of prostacyclin, a prostaglandin that increases vascular permeability and lowers blood pressure, may have an important physiologic role.

Changes in pulmonary function during the diuretic phase of respiratory distress syndrome.

To evaluate the relationship between improvement in pulmonary function and spontaneous diuresis in respiratory distress syndrome, nine premature infants requiring mechanical ventilation for RDS were studied at a mean age of 11.9 hours prior to the onset of diuresis, at onset of diuresis, at maximum urine output (mean age 44.9 hours), and at 24 hours after maximum urine output. Prior to diuresis functional residual capacity decreased from mean +/- SEM of 16.2 +/- 2 to 13.3 +/- 1.2 ml/kg, and dynamic lung compliance decreased from 2.5 +/- 0.3 to 1.8 +/- 0.3 ml/cm H2O (P less than 0.05), indicating that the respiratory disease was worsening. There was no significant change in alveolar-arterial oxygen gradient, peak inflating pressure, or rate of intermittent mandatory ventilation over this period. At the time of maximum urine output, however, FRC had increased 36% (P less than 0.05). CL had increased by 60% to 2.8 +/- 0.4 ml/cm H2O (P less than 0.025), AaDO2 had decreased from 246 +/- 27 to 184 +/- 30 torr (P less than 0.005), and PIP had decreased from 14.9 +/- 2.2 to 11.3 +/- 2.1 cm/H2O (P less than 0.05). On follow-up study 24 hours after maximum urine output, there was no further significant improvement in FRC, CL or PIP, but IMV rate and AaDO2 continued to decrease. These data show that the pulmonary function in RDS deteriorates until the onset of diuresis, after which it rapidly improves. This diuresis may represent the removal of excess lung liquid and seems necessary for improvement in RDS.