Uteroplacental dysfunction and prostaglandin metabolism in zinc deficient pregnant rats.
Relationships between perinatal mortality, disrupted utero-placental function and prostaglandin metabolism have been studied in Zn-deficient rats. Uterine contractility in vitro, placental blood flow in vivo, and uterine and placental prostaglandin synthesis from [1-14C] arachidonic acid in vitro were investigated at day 22 of pregnancy. High amplitude uterine contractions were almost completely eliminated and utero-placental blood flow was decreased by 85% by Zn deficiency. Synthesis of [1-14C]-prostaglandin E2, F2 alpha and 6-keto-F1 alpha from [1-14C] arachidonic acid decreased significantly in uterine tissue but increased in placentae. These possibly inter-related effects may contribute to the high perinatal mortality observed in Zn deficiency.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D005260:Female; D010920:Placenta / Q000098:blood supply / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D012039:Regional Blood Flow; D014590:Uterine Contraction; D014599:Uterus / Q000098:blood supply / Q000503:physiopathology*; D015032:Zinc / Q000172:deficiency*
D001095:Arachidonic Acids; D011453:Prostaglandins; D016718:Arachidonic Acid; D015032:Zinc