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Related Experiment Videos

Does human placenta produce prostacyclin?

J Y Jeremy, M A Barradas, I L Craft

    Placenta
    |January 1, 1985
    PubMed
    Summary
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    The human placenta has strong platelet anti-aggregatory activity, primarily due to its ADPase enzyme, not prostacyclin (PGI2). This study confirms placental tissue does not significantly produce PGI2.

    Area of Science:

    • Biochemistry
    • Reproductive Biology
    • Hematology

    Background:

    • Human placenta exhibits significant platelet anti-aggregatory activity.
    • This activity is specific to adenosine diphosphate (ADP)-induced aggregation.
    • Previous findings suggested placental extracts degrade ADP, implicating an 'ADPase' enzyme.

    Purpose of the Study:

    • To investigate whether human placental tissue synthesizes prostacyclin (PGI2).
    • To determine the source of the placenta's potent in vitro platelet anti-aggregatory activity.
    • To reconcile conflicting reports on placental PGI2 production.

    Main Methods:

    • Incubation of human placental and membrane tissues with [14C]-arachidonic acid to assess conversion to 6-oxo-PGF1 alpha.
    • Radioimmunoassay (RIA) techniques to quantify spontaneous 6-oxo-PGF1 alpha production.

    Related Experiment Videos

  • Platelet aggregation assays using various inducers (ADP, adrenaline, ristocetin, collagen).

    • Main Results:

    • Human placental and membrane tissues showed negligible conversion of [14C]-arachidonic acid to 6-oxo-PGF1 alpha.
    • Radioimmunoassay confirmed minimal spontaneous production of 6-oxo-PGF1 alpha by the placenta.
    • The placenta's anti-aggregatory effect was observed only with ADP-induced aggregation, not with other agents.

    Conclusions:

    • Human placental tissue and fetal membranes do not synthesize significant amounts of prostacyclin (PGI2).
    • The potent in vitro platelet anti-aggregatory activity of the human placenta is likely attributable to its ADPase activity.
    • The findings clarify the mechanism behind placental anti-platelet effects, distinguishing it from PGI2-mediated actions.