Effect of Hypoxia on Renal Prostaglandin E₂ Production in Human and Rat Neonates

Abstract

Effect of hypoxia on renal prostaglandin E₂ (PGE₂) production was shown in asphyxic newborn infants and experimental hypoxic rats. In asphyxic infants, at postnatal day 1, the urinary excretion of PGE₂ in severe asphyxia (1.00 ± 0.19 pg/kg/min, n = 10) was lower than that of the mild asphyxia (2.15 ± 0.18 pg/kg/min, n = 10) or normal newborn infants (2.65 ± 0.25 pg/kg/min, n = 8) (p < 0.01). The urinary excretion of PGE₂ was inversely correlated with the urinary N-acetyl-Β-D-glucosaminidase (r = ––0.84, p < 0.01). The urine volume in mild asphyxia (0.04 ± 0.005 ml/kg/min) was higher in comparison to normal newborn infants (0.026 ± 0.002 ml/kg/min) (p < 0.01), but had no correlation with the urinary excretion of PGE₂. In experimental hypoxic rats, the renal PGE₂ concentration increased from 0.19 ± 0.02 ng/mg protein to the maximum level of 0.59 ± 0.03 ng/mg protein at 10 min of hypoxia. The renal PGE₂ concentration then decreased to the minimum level (0.105 ± 0.02 ng/mg protein) at 24 h after 20 min hypoxia. The renal ATP rapidly decreased during 20 min hypoxia, and gradually increased to 55.1 ± 6.2 nmol/mg protein at 24 h after 20 min hypoxia, which recovered only about 60% of the control level. It seems likely that renal PGE₂ does not play a major role in diuresis in mild birth asphyxia and that severe birth asphyxia suppresses the renal PGE₂ production in early neonatal period. This suppression of the renal PGE₂ production may cause deterioration of the renal function after severe asphyxia. The delayed recovery of ATP may affect the renal PGE₂ concentration after hypoxia.

Compartmental Study of Rat Renal Prostaglandin Synthesis during Development

“…Hyp oxia is one of the conditions where most tis sues respond with an increase of prostaglan din synthesis [30]. However, in agreement with our results, it has been reported that uri nary excretion of PGE2 in asphyxic infants at day 1 is not higher than that of normal new born infants [31] reflecting that the renal PG system is insensitive to hypoxia during the perinatal period. No data are available about the prostaglandin response to the transient hypoxemia stress of the neonate, but no rise in PGs is expected to occur.…”

Developmental changes in cyclo‐oxygenase mRNA induction by hypoxia in rat kidney

“…If this situation is similar in human infants, lack of COX‐2 induction might help to explain why transient renal dysfunction is not uncommon after neonatal asphyxia. However, Suzuki and Togari reported that renal prostaglandin E 2 (PGE 2 ) does not play a major role in diuresis in mild birth asphyxia 38 . Our result was compatible with this view.…”