Enhanced reactivity of the platelet thromboxane pathway in normotensive and hypertensive pregnancies with insufficient fetal growth.
The reactivity of the platelet thromboxane pathway was investigated by means of measurement of thrombin-induced formation of malondialdehyde in platelets obtained from 26 women in the third trimester of uncomplicated pregnancies, 27 patients with normotensive pregnancies who were delivered of small--for--gestational age infants, 27 patients with pregnancy-induced hypertension and infants with normal birth weights, and 20 patients with pregnancy-induced hypertension and small--for--gestational age infants. Platelet life span and distribution of platelet volumes were also determined. In normotensive and hypertensive pregnant women with small--for--gestational age infants, platelet malondialdehyde formation was significantly increased, and platelet life span was reduced as compared with the other groups. The enhanced reactivity of the platelet thromboxane pathway may be expected to contribute to the increased in vivo platelet activation and consumption which occur in pregnancies with chronic placental insufficiency. Deficient production of placental vascular prostacyclin might be the underlying cause.
D001792:Blood Platelets / Q000378:metabolism*; D002470:Cell Survival; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood / Q000150:complications*; D006801:Humans; D008315:Malondialdehyde / Q000097:blood; D010976:Platelet Count; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000097:blood*; D011263:Pregnancy Trimester, Third; D013928:Thromboxane A2 / Q000378:metabolism*; D013931:Thromboxanes / Q000378:metabolism*
D013931:Thromboxanes; D008315:Malondialdehyde; D013928:Thromboxane A2