Prostaglandin I2 is less relaxant than prostaglandin E2 on the lamb ductus arteriosus

Coceani, Flavio; Bodach, E.; White, E.; Bishai, Isis; Olley, Peter M.

doi:10.1016/0090-6980(78)90051-5

Cited by 55 publications

(16 citation statements)

References 15 publications

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“…Previous comparisons of the relative efficacy of different prostaglandins as dilators of the ductus, both in vitro (Clyman et al, 1978;Coceani et al, 1978) and in vivo (Friedman et al, 1983) have been in the presence of indomethacin and it was on the basis of these studies that PGE1 was selected to be used to maintain artificially ductal patency in neonates with ductus-dependent circulation. It seems likely, therefore, that comparing the effects of different prostaglandins in the presence of indomethacin as a guide to their potency in the human infant with ductus-dependent circulation has led to two sources of error: (1) the sensitivity of the vessel to PGE1 was overestimated as the effects of endogenous PGE2 have been eliminated; and, (2) the sensitivity of the vessel to prostacyclin was underestimated, due to the absence of its potentiation by endogenous PGE2.…”

Section: Discussionmentioning

confidence: 99%

“…Indomethacin increases the sensitivity of the ductus arteriosus to PGE2, which has been postulated to be due to an effect of the drug's action on the PGE2 'target site' (Coceani et al, 1975 (Clyman et al, 1978;Coceani et al, 1978) and in vivo (Friedman et al, 1983). If indomethacin increases ductal sensitivity to PGE2, this may have exaggerated the sensitivity of the ductus to PGE2 relative to other prostaglandins.…”

Section: Introductionmentioning

confidence: 99%

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Interactions between indomethacin, noradrenaline and vasodilators in the fetal rabbit ductus arteriosus

Smith

McGrath

1994

British J Pharmacology

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1 Interactions between indomethacin, noradrenaline and vasodilators were studied in rings of ductus arteriosus isolated from fetal rabbits. The effect of incubation with prostaglandin E2 (PGE2) on the noradrenaline concentration-contraction response curve was studied in the presence and absence of indomethacin. Also, the ductus was pre-contracted with 10 fLM noradrenaline and concentrationrelaxation response curves (CRRC) to PGE2, cicaprost, cromakalim and forskolin were obtained in the presence and absence of indomethacin.2 In the absence of indomethacin, PGE2 (from 1 nM to 100 nM) decreased the pECM to noradrenaline to a maximum of 0.4 to 0.5 log units (i.e. an approximately three fold increase in EC50 [M]). In the presence of 1 j.M indomethacin, PGE2 (0.1 nm to 100 nM) decreased the pECm4 to noradrenaline by 2.39 log units (i.e. a 245 fold increase in ECm). By comparing the control pECm to noradrenaline with the relationship between the pEC_% to noradrenaline and [PGE2] in 1 glM indomethacin, the effect of endogenous PGE2 synthesized in the vessel wall was estimated as being equivalent to a bath concentration of approximately 1 nM exogenous PGE2. 3 When the vessel was pre-contracted with 1O gM noradrenaline, indomethacin had no effect on the CRRC to PGE2 but did alter the CRRC to other vasodilators. The sensitivity of the vessel to cicaprost, cromakalim and forskolin was decreased in 1 1M indomethacin compared with control. Forskolin caused complete relaxation in the presence and absence of indomethacin. Indomethacin decreased the maximum response to cromakalim but increased the maximum response to cicaprost. PGE2, 0.3 nm, partially reversed the effect of indomethacin on the sensitivity of the vessel to forskolin. 4 We conclude that under varying experimental conditions, indomethacin increased the sensitivity of the ductus to the effects of PGE2 but decreased its sensitivity to other vasodilators. Both effects can be explained by elimination of endogenous PGE2. However, indomethacin increased the maximum response to cicaprost, which cannot be explained by elimination of endogenous PGE2 but may be due to elimination of endogenous prostacyclin.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interactions between indomethacin, noradrenaline and vasodilators in the fetal rabbit ductus arteriosus

Smith

McGrath

1994

British J Pharmacology

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“…In our case, intensive fetal surveillance during intravenous epoprostenol therapy failed to show fetal harm. Epoprostenol causes vasodilation of the ductus arteriosus, 25 but given its short half-life, 19 would be unlikely to have neonatal effects.…”

Section: Discussionmentioning

confidence: 99%

Epoprostenol treatment for idiopathic pulmonary arterial hypertension in pregnancy

et al. 2010

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Idiopathic pulmonary arterial hypertension is a rare condition associated with significant maternal mortality. We report the management of a 37-year-old multigravida with severe disease using epoprostenol, a multidisciplinary approach, and a planned delivery. Although the patient survived the pregnancy, her pulmonary function significantly worsened. Epoprostenol, a pulmonary vasodilator, should be considered when indicated during pregnancy. Neither fetal nor neonatal harm was identified.

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“…A critical player in regulating intimal thickening PGE 2 , the most potent vasodilator affecting the DA, is produced in the placenta (Smith 1998) and in the DA itself (Clyman, 1978;Coceani, 1978). During gestation, PGE 2 contributes to DA patency in utero.…”

Section: Pge 2 -Ep4mentioning

confidence: 99%

Recent Advances Concerning the Molecular Mechanism of Patent Ductus Arteriosus

Minamisawa¹,

Yokoyama²

2012

Congenital Heart Disease - Selected Aspects

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Prostaglandin I2 is less relaxant than prostaglandin E2 on the lamb ductus arteriosus

Cited by 55 publications

References 15 publications

Interactions between indomethacin, noradrenaline and vasodilators in the fetal rabbit ductus arteriosus

Interactions between indomethacin, noradrenaline and vasodilators in the fetal rabbit ductus arteriosus

Epoprostenol treatment for idiopathic pulmonary arterial hypertension in pregnancy

Recent Advances Concerning the Molecular Mechanism of Patent Ductus Arteriosus

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