PROSTAGLANDINS PROSTACYCLYN AND HUMAN FOETAL CII~UIATION G.~zZl , R±MiSlanl ,~D.Yg/ratore , D. Marchesl ,M.LlVlQ , A. Schleppati , G.Me~ , G.de Gaetanc~ and M.B.Donatl~ D e ~ t of Nephrology and Dialysis and ~Department of Obstetrics and Gynecology II,Ospedali Riuniti, BERGAMO,Italy and ~Istituto di Ricerche Farmaoologiche 'Mario Negri',~, Italy ABSTRACT Tissues frc~ human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels frc~ normal adults. High prostacyclin generation could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation in which blood pressure is low despite very high cardiac output. ~DUCTION Foetal circulation is characterized by high cardiac output and low blood pressure (1,2) . ~is is related to the low oxygen saturation of foetal blood and is possible because of low total vascular resistance (2). Mechanis~s underlying peripheral vasodilation in the foetus are unknown, but prostaglandins have been suggested as playing a role in the regulation of vascular tone (3). Foetal bovine vascular tissues (2,4,5) and ht~retnendothelial cells in culture (4) generate prostacyclin (PGI9) frc~ exogenous arachidonic acid; this prosta- glandin has poten£ vasodilatory properties and antiplatelet aggrega- tion activity. We have studied prostacyclin activity in human umbilical and placental vessels obtained at the end of uncomplicated pregnancy. MATEP/ALS AND ~fHODS SpecLmem~ of umbilical and placental vascular tissue were obtained immediately after the expulsion of placenta at the end of uncc~pli- cated pregnancy frc[n eleven healthy women (aged 18-34). Eight were primigravidae and 3 secundiparae. They all gave informed consent. None of these subjects had received any blood transfusion or drug known to affect prostaglandin metabolism in the month prior to the study,and they all stated they took no aspirin or aspirin-like drugs. Blood pressure, urinalysis, proteinuria,clearance of creatinine and uric acid, haematocrit,platelet count and sert~n fibrinogen degrada- SEPTEMBER 1979 VOL. 18 NO. 3 341