Prostaglandin E2 in the lung lavage fluid of premature newborns before and after surgical or medical closure of a patent ductus arteriosus

Strasser, Th.; Vogel, Margot

doi:10.1016/0005-2760(89)90099-4

Cited by 3 publications

(2 citation statements)

References 9 publications

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“…Circulating PGE 2 is thought to play an important role in the patency of the DA [6]. Infants with PDA have significantly higher circulating PGE 2 than normal preterm infants of the same age [15], and PGE 2 levels were observed to be significantly decreased after the surgical or medical treatment of PDA [20]. Considering these reports, the present findings suggest that ACEIs increase the sensitivity of the DA to PGE 2 and may contribute to PDA after ACEIs therapy.…”

supporting

confidence: 51%

Enhancement of Neonatal Rat Ductal Responsiveness to Prostaglandin E2 after Maternal Treatment with Enalapril or Captopril.

Togashi

Takizawa

Kawahata

et al. 1998

The Journal of Veterinary Medical Science

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ABSTRACT. This work was conducted to determine whether the angiotensin-converting enzyme inhibitors (ACEIs) (enalapril and captopril) administered to mother rats prenatally can potentiate a re-opening of the neonatal ductus arteriosus (DA) induced by prostaglandin E 2 (PGE 2 ) after postnatal closure. A subcutaneous injection of PGE 2 (4 µg) was administered to newborn rats 3 hr after a Cesarean delivery from females which had been orally given 0.1, 1 or 10 mg/kg/day of enalapril or 15 or 150 mg/kg/day of captopril from day 14 to day 20 of gestation. The ratio of the DA to the pulmonary artery (PA) was determined at intervals after the injection. The DA/PA ratio was significantly higher in the newborn rats of mothers who were transplacentally administered these agents compared to the controls, except at the low dose (0.1 mg/kg) group of enalapril. We found that the level in the neonatal lungs of 15-hydroxy prostaglandin dehydrogenase, a key enzyme that catalyzes PGE 2 to convert it to its inactive metabolite 15-keto-PGE 2 , was not affected after maternal treatment with enalapril or captopril. These results indicate that the increased ductal responsiveness to PGE 2 in newborn rats was a common response after maternal ACEI treatment, but the catabolism of PGE 2 in the lungs did not contribute to this response. -KEY WORDS: ductus arteriosus, PGE 2 catabolism, re-opening.J. Vet. Med. Sci. 60(8): 989-991, 1998 that the maternal administration of ACEIs such as enalapril and captopril can potentiate the neonatal ductal responsiveness to PGE 2 after the postnatal closure of the DA and can inhibit the catabolism of PGE 2 in the lungs. We investigated the effects of enalapril and captopril on the re-opening of the DA as well as the effect of these agents on the activity in the lungs of 15-hydroxy prostaglandin dehydrogenase (15-PGDH), a key enzyme which catalyzes the initial reactions converting the biologically active PGE 2 to its inactive metabolite, 15-keto-PGE 2 .Female Crj: Wistar rats, 10-12 weeks old at the time of mating, were used. They were maintained on a commercial diet (CE-2, Clea Japan, Tokyo) and tap water ad libitum, and kept in a room at a temperature of 22 ± 3°C with a relative humidity of 55 ± 10%. Three females were placed with a male overnight and examined the next morning for the presence of sperm in the vaginal smear. The day on which sperm was found was designated as day 0 of gestation, and the females were caged individually thereafter.In the first experiment, the effects of prenatal enalapril and captopril treatments on the re-opening of the DA induced by PGE 2 was examined. Enalapril (0.1, 1, 10 mg/ kg/day) or captopril (15, 150 mg/kg/day) administration was carried out from day 14 to day 20 of gestation. Pregnant females given only saline served as the controls. The rats were killed by decapitation at 1 p.m. on day 21 of gestation at least 24 hr after the last drug administration, and the newborn pups were immediately obtained by Cesarean delivery. Only male pups were used in this study. Th...

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supporting

confidence: 51%

Enhancement of Neonatal Rat Ductal Responsiveness to Prostaglandin E2 after Maternal Treatment with Enalapril or Captopril.

Togashi

Takizawa

Kawahata

et al. 1998

The Journal of Veterinary Medical Science

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“…11 Local concentrations of both PGE2 and TxB2 in tracheal lavage fluid were significantly lower in a small cohort of preterm infants treated with indomethacin during the first week as well as within a few hours following surgical ligation. 24,25 We examined the effect of antenatal steroids as an alteration in prostanoid synthesis has been speculated to be a steroid effect but we did not find any difference.…”

Section: Discussionmentioning

confidence: 84%

Chorioamnionitis and Ontogeny of Circulating Prostaglandin and Thromboxane in Preterm Infants

et al. 2008

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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.

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Inhibitory effect of indomethacin on neonatal lung catabolism of prostaglandin E2: possible mechanism of the reopening of the ductus arteriosus after indomethacin therapy.

Takizawa

Ikeda²,

Togashi³

et al. 1996

J. Toxicol. Sci.

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Prostaglandin E2 in the lung lavage fluid of premature newborns before and after surgical or medical closure of a patent ductus arteriosus

Cited by 3 publications

References 9 publications

Enhancement of Neonatal Rat Ductal Responsiveness to Prostaglandin E2 after Maternal Treatment with Enalapril or Captopril.

Enhancement of Neonatal Rat Ductal Responsiveness to Prostaglandin E2 after Maternal Treatment with Enalapril or Captopril.

Chorioamnionitis and Ontogeny of Circulating Prostaglandin and Thromboxane in Preterm Infants

Inhibitory effect of indomethacin on neonatal lung catabolism of prostaglandin E2: possible mechanism of the reopening of the ductus arteriosus after indomethacin therapy.

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