Thromboxane and Prostacyclin Levels in Fetal Rabbit Brain and Placenta After Intrauterine Partial Ischemic Episodes

The appearance of arachidonic acid (AA) oxidation products in fetal rabbit brain and placenta under normal or partial short‐term ischemic episodes induced by placental blood vessel restriction was examined. Intracerebral administration of [³H]AA into close‐to‐term rabbit fetuses gave rise to radioactively labeled prostaglandin (PG) E₂, thromboxane B₂, and 6‐keto‐PGF₁ metabolites as detected by HPLC analysis. A significant increase of 20–30% of [³H]AA precursor into eicosanoids was detected in brain of fetuses after 2‐h restriction. The thromboxane B₂ and 6‐keto‐PGF₁ levels were determined by radioimmunoassay technique over a period of 48 h following ischemic episodes. Thromboxane B₂ content in affected animals was higher by five‐ and twofold at 3 h over control fetal brain and placental tissue values, respectively, and remained significantly high for 24 h. 6‐Keto‐PGF₁ levels reached a peak value that was greater by 2.5‐ and 1.5‐fold at 6 h for the ischemic brain and placental tissue, respectively, compared with control fetuses. PGE₂ levels were less affected, attaining a maximum of 1.9‐ and 1.1‐fold in brain and placenta correspondingly. The thromboxane/prostacyclin ratio reached a maximum in the brain after ∼3 h, while that in the placenta continued to rise even after 20 h. Persisting high levels of thromboxane are indicative of cerebral vasoconstriction and may suggest possible damaging effects.