The timing of parturition in the pig is altered by intravenous naloxone

This experiment tested the hypothesis that opioid antagonists could influence the timing of the onset and progress of parturition in the pig. Primiparous pigs (gilts) received a jugular catheter on Days 104 to 106 of pregnancy. At 1400 h on Day 112 the gilts received 10 mg PGF2alpha, im to induce parturition. At 1000 h on Day 113 (i.e., 20 h later) gilts received either saline (n = 6), 1 mg/kg, iv naltrexone (n = 4) or 1 mg/kg, iv naloxone (n = 5). Blood samples were taken daily from Days 108 to 116. On Day 113, blood samples were taken hourly from 0500 to 0900 h and then every 30 min until 2400 h, or until the birth of the last piglet (BLP) (whichever was sooner) and assayed for progesterone, oxytocin (OT), cortisol and PRL. Additional blood samples for OT and cortisol assay were taken every minute from 0930 to 1100 h on Day 113 and for 30 min during parturition. Naloxone, but not naltrexone, delayed the onset of parturition relative to saline controls (by 14 h 21 min; P < 0.05). Duration of parturition and rate of births were not significantly affected by treatment. Mean plasma OT increased in the 4 h following naloxone but not saline treatment, during which time OT plasma pulse amplitude was reduced in naloxone and naltrexone-treated animals relative to saline treated controls. The PRL secretion rose following treatment in saline treated animals, consistent with approaching parturition, but failed to rise in opioid antagonist treated animals. Progesterone concentrations remained elevated in naloxone-treated animals for longer than in the other groups. These data suggest that a rapid change in overall effect of parenteral administration of naloxone to parturient pigs occurs from delaying its onset when administered as in these experiments, to facilitating its progress when given during parturition (earlier experiments). The delay of onset of parturition may be mediated by interference with hypothalamic control of OT or PRL release. (C) 2000 by Elsevier Science Inc.