Prostacyclin-Like Activity Of Amniotic Fluid In Preeclampsia

Abstract

Studies have been undertaken to compare amniotic fluid from patients with pre-eclampsia (PET) with normotensive controls in inhibiting platelet aggregation (PGI2-like activity) and accelerating coagulation tests. After 39 weeks of gestation, samples from PET patients showed significantly less PGI2-like activity (p<0.001) and significantly lower kallikrein levels (p<0.01) than normotensive controls. These findings suggest that the biosynthesis and release of these substances may be impaired in PET. In view of the association of PET with intravascular clotting, the highly significant reduction of PGI2-like activity appears important and warrants a clinical trial of prostacyclin administration in this disorder.

Plasma and Amniotic Fluid Prostacyclin and Thromboxane in Mild Pregnancy-Induced Hypertension

“…In the present study, plasma and amniotic fluid concentrations of 6 keto PGFj alpha in subjects with mild PIH did not differ significantly from those of control normo tensive subjects. This finding for mild PIH is consistent with amniotic fluid data reported by Ylikorkala 15 and suggests that suppression of PGI 2 probably is not a primary change in the pathogenesis of mild PIH.…”

A clinical trial of a slow‐release formulation of acetylsalicylic acid in patients at risk for preeclampsia.

“…In preeclampsia, however, more TXA2 is produced than prostacyclin (Walsh, 1985). Prostacyclin activity has also been found to be lowered significantly in amniotic fluid in preeclampsia (Bodzenta et al, 1981). A balance between thromboxane A2 and prostacyclin in preeclampsia appears to be obtained by use of low-dose acetylsalicylic acid but the optimal dose of acetylsalicylic acid to prevent preclampsia is unclear.…”

Decreased prostacyclin production by placental cells in culture from pregnancies complicated by fetal growth retardation

“…Recently, attention has been focused on prostacyclin (PGIJ a potent platelet anti-aggregatory prostanoid. 1980) or placental (Remmuzzi et al 1980) tissue may be a factor in the development of the pathophysiological change of pregnancy-induced hypertension with or without fetal growth retardation (Bodzenta et al 1980;Lewis et al 198 1) Umbilical arteries from small-for-datesinfants have a reduced capacity to synthesize PGI, in vitro (Stuart et al 1981 shown to possess prostacyclin-like activity (Myatt & Elder 1977) and to produce 6-0x0-prostaglandin(PG)F,,, the stable hydrolysis product of PGI, (Mitchell et al 1978). 1980) or placental (Remmuzzi et al 1980) tissue may be a factor in the development of the pathophysiological change of pregnancy-induced hypertension with or without fetal growth retardation (Bodzenta et al 1980;Lewis et al 198 1) Umbilical arteries from small-for-datesinfants have a reduced capacity to synthesize PGI, in vitro (Stuart et al 1981 shown to possess prostacyclin-like activity (Myatt & Elder 1977) and to produce 6-0x0-prostaglandin(PG)F,,, the stable hydrolysis product of PGI, (Mitchell et al 1978).…”

“…Reduced PGI, production by maternal (Bussolino et al 1980), fetal (Downing et a/. 1980) or placental (Remmuzzi et al 1980) tissue may be a factor in the development of the pathophysiological change of pregnancy-induced hypertension with or without fetal growth retardation (Bodzenta et al 1980;Lewis et al 198 1) Umbilical arteries from small-for-datesinfants have a reduced capacity to synthesize PGI, in vitro (Stuart et al 1981).…”