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Biomedical subjects

G Jenkin

Publications and source records attributed to G Jenkin.

96 records · Page 6Linked to original sources
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Effects of luteolytic doses of prostaglandin F2 alpha and cloprostenol on concentrations of progesterone, luteinizing hormone, follicle-stimulating hormone, glucose, insulin, growth hormone, thyroxine, prolactin and cortisol in jugular plasma of lactating dairy cows.

Three groups of five lactating dairy cows in the mid-luteal phases of oestrous cycles were given an injection (at time 0 h) of the naturally-occurring prostaglandin F2 alpha (PGF2 alpha) or cloprostenol (a synthetic analogue of PGE2 alpha) at doses recommended for inducing luteolysis, or injection vehicle. Concentrations of glucose and hormones in jugular plasma were measured from 26 h before to 12 h after the injections and the significance (P < 0.05) of the effects of the prostaglandins on these concentrations was determined. Both prostaglandins induced falls in progesterone concentration and rises in luteinizing hormone concentration; neither influenced follicle-stimulating hormone. PGF2 alpha increased glucose concentration; neither prostaglandin influenced insulin concentration. Both prostaglandins increased growth hormone concentration and resulted in declining thyroxine concentration. PGF2 alpha increased prolactin and cortisol concentration. There were, however, no significant differences between the effects of the two prostaglandins on any hormone (or glucose) concentration.

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Inhibition of prostaglandin synthesis and its effect on uterine activity during established premature labor in sheep.

OBJECTIVE: Continuous infusion of the selective prostaglandin synthase type-2 inhibitor nimesulide, together with the oxytocin receptor antagonist atosiban, inhibits glucocorticoid induction of labor in sheep. We evaluated the effectiveness of this treatment commencing after the onset of premature labor when prostaglandin concentrations are already significantly elevated. METHODS: Premature labor was induced in chronically cannulated fetuses by constant fetal dexamethasone infusion. After the onset of active labor in each ewe, defined as uterine electromyographic (EMG) activity twice basal levels, ewes received combined nimesulide and atosiban (20.0 and 4.12 mg/kg per day, respectively; n = 6) or vehicle (n-methyl-2-pyrrolidone and saline each 1 mL/hour; n = 4) infusions for 48 hours. Maternal and fetal plasma PGFM (13,14-dihydro-15-keto PGF2alpha, the stable metabolite of prostaglandin (PG) F2alpha) and PGE2 concentrations were measured before, during, and after infusions. RESULTS: Four nimesulide- and atosiban-treated ewes successfully completed the 48-hour infusion period with no deliveries occurring during inhibitor treatment, or up to 6 hours after inhibitor treatment. Delivery was delayed in two other ewes, compared with control animals. Uterine EMG activity in nimesulide- and atosiban-treated ewes (n = 4) was significantly reduced during the 48-hour inhibitor treatment period. Maternal and fetal prostaglandin concentrations were significantly decreased in inhibitor-treated ewes during and after the infusions. CONCLUSIONS: The combination of nimesulide and atosiban treatment for 48 hours successfully inhibited the progression of active premature labor to delivery. This study further supports the potential value of this treatment regime for the inhibition of premature labor.

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Effect of oxytocin and estradiol on uterine prostaglandin release in nonpregnant and early-pregnant ewes.

The effects of exogenous oxytocin (OT) and estradiol-17 beta (E2) on plasma concentrations of prostaglandin (PG) E2 and 13, 14-dihydro-15-keto-PGF2 alpha (PGFM) were investigated on Day 14-15 (NP) of the estrous cycle and Days 14-16 (PI) and 21-25 (EP) of pregnancy in the ewe. Basal concentrations of PGFM were significantly elevated in utero-ovarian venous (UOV) plasma on Day 14 of pregnancy (4.05 +/- 0.81 nM, mean +/- SEM) compared to that observed on Day 14 of the cycle or Days 21-25 of pregnancy (2.29 +/- 1.3 nM and 1.06 +/- 0.56 nM, respectively). PGFM release increased significantly following intera-arterial bolus injections of 50, 500, and 5000 mU OT at 2-h intervals in all experimental groups. There was no significant difference in area and peak height of the PGFM response between the 3 groups studied. The time to peak PGFM response was, however, significantly longer in the PI group. No significant changes in concentration of PGFM were observed in any experimental group following 1-h infusions of E2 at 5, 50, and 500 pmol/min. Long-term (15-18 h) infusion of E2 at 83 pmol/min increased the peak height of the OT-induced PGFM response at both stages of gestation studied. PGE2 concentrations in UOV plasma were less than 0.05 nM in all samples studied. These results demonstrate that PG release can be induced in response to OT during the period in which ovine trophoblastic protein-1 (oTP-1) is released by the conceptus. During pregnancy, oTP-1 does not appear to inhibit the E2 induction of uterine OT receptors.

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