Bakker W W, Timmerman W, Poelstra K, Schuiling G A
Department of Pathology, Obstetrics and Gynaecology, University Hospital of Groningen, The Netherlands.
Placenta. 1992 May-Jun;13(3):281-90. doi: 10.1016/0143-4004(92)90043-s.
The mechanism underlying increased sensitivity for endotoxin in pregnancy, as reflected by intravascular thrombus formation in various organs i.e. the placenta, is unknown. We studied the influence of endotoxin infusion at day 14 upon the vascular antithrombotic ADPase present in the labyrinth of the rat placenta just before term (day 21). Pregnant Wistar rats were infused with either endotoxin (1 microgram/kg body weight) or saline through permanent vena jugularis catheters and their placenta and kidneys were examined at day 21 using light electron microscopy and enzyme cytochemistry at the ultrastructural level. Also, placenta perfusion ex vivo was done using platelets and ADP to test the thrombotic tendency of placental vessels in endotoxin treated and control rats. The results show in both maternal as well as the fetal vessels of the placental labyrinth vascular occlusions and decreased membrane ADPase activity exclusively in endotoxin treated and not in saline infused pregnant animals. Alternate placenta and kidney perfusion ex vivo resulted in intraplacental and intraglomerular platelet aggregation again exclusively in endotoxin-treated rats. It is concluded that vascular ADPase may be affected by endotoxin due to the pregnant condition, resulting in a functional defect in antithrombotic potention which may promote intravascular formation of microthrombi in situ.
