抄録
Prostaglandin E2 (PGE2), thromboxane B2 (TXB2; as a stable metabolite of TXA2), prostaglandin F2α(PGF2α) and 6-keto-PGF1α(as a stable end product of prostacyclin) have been measured by using specific radioimmunoassay in the plasma of the cord artery immediately after delivery before the cord was clamped. Plasma prostanoid concentrations in normal deliveries (n=8, as controls) were 24.8±2.6 (PGE2), 246.8±37.0 (TXB2), 122.2±13.3 (PGF2α) and 82.1±7.7 (6-keto-PGF1α) respectively (pg/ml, mean±s.e). On the other hand, in fetal distressed deliveries showing continuous bradycardia (n=6), they increased significantly to 275.4±20.1 (PGE2), 948.6±102.5 (TXB2), 218.0±21.4 (PGF2α) and 1498.6±298.4 (6-keto-PGF1α) respectively (pg/ml, mean±s. e, p<0.005). However, both PGF2α/PGE2 and TXB2/6-keto-PGF1α ratios declined significantly from 4.70±0.33 to 0.68±0.05 and from 3.07±0.37 to 0.68±0.12 respectively (mean±s. e, p<0.005) in the fetal distressed group compared with those of the controls. From these results, it may be concluded that the cord artery, which is known as the patent source for the production of PGE2 and prostacyclin, did exert a sufficiently strong reaction to overcome the undesirable haemodynamic changes to maintain the fetal well-being in utero.
