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Lung eicosanoids in perinatal rats with congenital diaphragmatic hernia
H Ijsselstijn1, F J Zijlstra, J P Van Dijk
1Department of Paediatric Surgery Division of Respiratory Medicine Erasmus University Rotterdam and University Hospital/Sophia Children's Hospital Dr. Molewaterplein 60 Rotterdam 3015 GJ The Netherlands.
Insights
Infants with congenital diaphragmatic hernia (CDH) show abnormal pulmonary eicosanoid levels. Elevated levels of the vasodilator prostacyclin (PGI(2)) may compensate for increased vascular resistance in CDH.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Biochemistry
Background:
- Abnormal pulmonary eicosanoid levels are observed in persistent pulmonary hypertension (PPH) and congenital diaphragmatic hernia (CDH).
- A potential dysregulation of vasoconstrictive and vasodilatory eicosanoids may contribute to PPH in CDH patients.
Purpose of the Study:
- To investigate the hypothesis that a dysbalance of vasoconstrictive and vasodilatory eicosanoids is involved in PPH in CDH patients.
- To measure and compare eicosanoid levels in control and CDH rat models.
Main Methods:
- Eicosanoid levels (6-keto-PGF(1alpha), TxB(2), PGE(2), LTB(4)) were measured in lung homogenates and bronchoalveolar lavage fluid.
- Measurements were performed in control rats and rats with CDH after caesarean section or spontaneous birth.
Main Results:
- In control rats, concentrations of 6-keto-PGF(1alpha), TxB(2), PGE(2), and LTB(4) decreased after spontaneous birth.
- CDH pups exhibited respiratory insufficiency immediately after birth.
- CDH rat lungs showed higher levels of 6-keto-PGF(1alpha), a metabolite of the pulmonary vasodilator prostacyclin (PGI(2)), compared to controls.
Conclusions:
- Abnormal lung eicosanoid levels are present perinatally in CDH.
- Elevated 6-keto-PGF(1alpha) levels in CDH may represent a compensatory mechanism for increased pulmonary vascular resistance.
Abstract:
Abnormal levels of pulmonary eicosanoids have been reported in infants with persistent pulmonary hypertension (PPH) and congenital diaphragmatic hernia (CDH). We hypothesized that a dysbalance of vasoconstrictive and vasodilatory eicosanoids is involved in PPH in CDH patients. The levels of several eicosanoids in lung homogenates and in bronchoalveolar lavage fluid of controls and rats with CDH were measured after caesarean section or spontaneous birth. In controls the concentration of the stable metabolite of prostacyclin (6-keto-PGF(1alpha)), thromboxane A(2) (TxB(2)), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)) decreased after spontaneous birth. CDH pups showed respiratory insufficiency directly after birth. Their lungs had higher levels of 6- keto-PGF(1alpha), reflecting the pulmonary vasodilator prostacyclin (PGI(2)), than those of controls. We conclude that in CDH abnormal lung eicosanoid levels are present perinatally. The elevated levels of 6-keto-PGF(1alpha) in CDH may reflect a compensation mechanism for increased vascular resistance.
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