Effect of finadyne on oestradiol-induced ovarian oxytocin and uterine PGF2alpha secretory systems on day 15 after oestrus in ovarian autotransplanted ewes.
This study was undertaken to determine whether induction of ovarian oxytocin after oestradiol treatment on day 15 after oestrus is mediated through prostaglandin secretion by blocking prostaglandin synthesis using finadyne, an inhibitor of the cyclo-oxygenase pathway. Nine ewes with ovarian autotransplants were assigned randomly to receive an i.m. injection of either oestradiol benzoate (50 microg) in peanut oil ( n= 5) or oestradiol benzoate plus finadyne (2.2 mg kg (-1)) ( n= 4) at 3 h intervals starting at the time of oestradiol injection. Blood samples were collected from the ovarian and contralateral jugular veins at 30 min intervals for 6 h before and at 15 min intervals for up to 9 h after the oestradiol and finadyne injections. The secretion rate of ovarian progesterone remained high in all ewes, thus indicating the presence of a functional corpus luteum. Peripheral oestradiol concentrations were significantly (P < 0.001) higher during the 9 h after oestradiol injection in both groups. None of the oestradiol-finadyne-treated ewes showed significant pulses in either ovarian oxytocin secretion or release of the prostaglandin F(2alpha) metabolite 13,14-dihydro-15-keto PGF(2alpha) (PGFM) after injections. In ewes treated with oestradiol only, at least one detectable pulse of ovarian oxytocin and jugular PGFM was observed with mean +/- SEM amplitude of 17.7 +/- 7.29 ng min (-1) and 237.18 +/- 43.13 pg ml (-1), respectively. The areas under the curve for ovarian oxytocin and jugular PGFM pulses were significantly increased after oestradiol treatment. These findings demonstrate that initiation of the arachidonic acid cascade is important for the secretion of oxytocin after oestrogen treatment.
Al-Matubsi
H Y
HY
College of Medicine, Department of Obstetrics and Gynecology, University of Cincinnati, PO Box 670526, Cincinnati, OH 45267-0526, USA. Hisham.Al-Matubsi@uc.edu
Fairclough
R J
RJ
D000818:Animals; D003002:Clonixin / Q000031:analogs & derivatives / Q000494:pharmacology*; D003338:Corpus Luteum / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism*; D004958:Estradiol / Q000031:analogs & derivatives / Q000097:blood / Q000494:pharmacology; D004971:Estrus; D005260:Female; D010053:Ovary / Q000187:drug effects* / Q000378:metabolism / Q000637:transplantation; D010121:Oxytocin / Q000378:metabolism*; D011374:Progesterone / Q000378:metabolism; D012756:Sheep; D014182:Transplantation, Autologous; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism
D016861:Cyclooxygenase Inhibitors; C074283:estradiol 3-benzoate; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D011374:Progesterone; D004958:Estradiol; D010121:Oxytocin; C014558:flunixin meglumine; D015237:Dinoprost; D003002:Clonixin