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The human placental anti-aggregating factor is neither prostacyclin, nor a prostacyclin metabolite
Authors:MJ Dembl-Duchesne  H Thaler-Dao  C Chavis  ACrastes de Paulet
Institution:Institut National de la Santé et de la Recherche Médicale - U. 58 60, Rue de Navacelles - 34100 Montpellier, France
Abstract:Using PGH2 as substrate, we have previously demonstrated that human placenta synthetizes mainly PGE2, TxB2 and PGD2(1,2). Other reports have shown that placental tissue generates a substance which inhibits ADP-induced platelet aggregation and which was supposed to be PGI2 (3). The present study indicates that the stability of that substance is different from the stability of prostacyclin (released by umbilical artery pieces). By GC-MS and multiple ion-monitoring, we have shown the presence of 6 keto-PGF (the stable metabolite of PGI2) in the umbilical artery incubation medium, while no trace of 6-keto-PGF could be found in the placental medium. No conversion of AA to 6-keto-PGF by placental microsomes was observed, even in the presence of antioxidants. The placenta possesses, in addition to the known 15-OH-PGDH and Δ-13 reductase activities, a weak 9 OH pGDH which is specific for PGF (and not PGI2 nor 6-keto-PGF). GC-MS analysis is showed that the expected metabolites of PGI2 through those three enzymes were not found in the placental medium, indicating that neither PGI2 synthesis nor metabolism could be demonstrated in the placenta.
Keywords:AA  arachidonic acid  ADP  adenosine diphosphate  DTT  dithiothreitol  GSH  reduced glutathione  MID  multiple ion detection  NAD  α-nicotinamide adenine dinucleotide  PG  prostaglandin  PGDH  prostaglandin dehydrogenase  PRP  platelet-rich plasma  s  d    standard deviation
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