EFFECT OF CONTINUOUS INFUSION OF OXYTOCIN ON PROSTAGLANDIN-F2-ALPHA SECRETION AND LUTEOLYSIS IN THE CYCLIC EWE

Circulating concentrations of 13, 14-dihydro-15-keto PGF2 α (DHKF2 α), luteinizing hormone (LH) and prolactin (PRL) have been measured in cyclic ewes treated with continuous infusions of oxytocin, in order to investigate the mechanism by which the treatment delays luteal regression. Continuous infusion of oxytocin reduced prostaglandin F2 α ((PGF2 α) secretion but had no detectable direct effect on LH or PRL. Oxytocin (3 nmol h-1 i.v.) given from Day 12 or 13 until Day 18 after oestrus delayed luteolysis, eight out of nine treated ewes not returning to behavioural oestrus until Day 29-1 ± 3.2 (mean ± s.e.m.; cycle length of Control ewes 16.7 ± 0.3 days). In the ewe in which oxytocin failed to prevent luteolysis, luteal regression had commenced before oxytocin treatment was started. In three ewes undergoing delayed luteolysis (cycle lengths, 21, 24 and 25 days) basal concentrations of PGF2a (measured as DHKF2 α) were unchanged, but there was only one episode of PGF2 α secretion compared with 20 episodes in three control ewes. Prolactin secretion was pulsatile during oxytocin infusion, and levels were low following infusion in ewes with cycle length >25 days while the corpora lutea were maintained. Circulating PRL concentrations were high in ewes undergoing delayed luteolysis but there was no discrete episode of PRL secretion associated with the pre-ovulatory LH surge in these animais. To investigate the possibility that the pattern of PGF2 α secretion was affected by depletion of oxytocin from corpora lutea, ewes previously treated with oxytocin to delay luteolysis were given a luteolytic dose of cloprostenol on Day 21 after oestrus. The amount of oxytocin secreted in response to cloprostenol was <10% of that seen in ewes similarly treated on Days 11-13 after oestrus. Low levels of luteal oxytocin may therefore reduce PGF2 α secretion in ewes undergoing delayed luteolysis. © 1990 CSIRO. All rights resreved.