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We studied the role of nitric oxide (NO) on the regulation of blood flow in the immature kidney during hypoxia, resuscitation and the recovery period using the NO inhibitor N(omega)-nitro-L-arginine (L-NNA) in a newborn piglet model, and the possibility of urinary cGMP as an index of renal function. After administration of L-NNA, the blood flow in both the cortex and medulla significantly decreased, indicating that NO is constantly released to maintain renal circulation. During hypoxia, the renal blood flow fell remarkably, and there were no differences between the control and L-NNA groups. During the post-resuscitation period, the recovery of renal blood flow was significantly suppressed in L-NNA administration, and it was speculated that NO might be an important factor for recovery of circulation from vasoconstriction due to hypoxemia. Urinary cGMP/cr was significantly increased on recovery from hypoxemia and was suppressed by L-NNA administration. This result suggested that the change in cGMP/cr represents renal blood flow change. We conclude that NO may play an important role in maintaining basal hemodynamics, and may also be a crucial factor for recovery from post-hypoxic vasoconstriction in premature kidneys. Urinary cGMP/cr might serve as one of the indices for assessment of premature renal circulation.

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 less than 0.01). The urinary excretion of PGE2 was inversely correlated with the urinary N-acetyl-beta-D-glucosaminidase (r = -0.84, p less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)