Ewe luteal function influenced by pulsatile administration of synthetic LHRH/FSHRH.

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The influence of repetitive administration of synthetic LHRH/FSHRH or saline (S) on 17beta-estradiol (E2)-induced precocious luteal regression in the ewe was examined. Ewes were pre-treated on days 10 and 11 of the estrous cycle with either 750 mug E2 (total dose = 1.5 mg) in oil or with oil (O) alone. Treatment involved in delivery of 10 mug of synthetic LHRH/FSHRH in saline or an equal volume of saline only, administered at 2-h intervals beginning on day 12 of the estrous cycle and continuing through the succeeding 72 hours. During the period of LHRH administration, the serum LH patterns in the O-LHRH and E2-LHRH groups were characterized by rhythmic fluctuation, rising in response to LHRH and falling prior to the subsequent treatment injection. Throughout the course of the treatment period, the serum LH levels in the O-LHRH group were consistently higher than those in the E2-LHRH group. No increase in serum LH concentration was observed in the saline-treated animals. The mean luteal weight and mean luteal progesterone content at the end of the 72-h period were not significantly different between the O-S and E2-LHRH groups (543 +/- 88 vs. 455 +/- 126 mg and 13.1 +/- 6.2 vs 16.0 +/- 9.7 mug, respectively). Both luteal weight and progesterone content were increased (P less than .01) in the O-LHRH group (1089 +/- 87 mg and 47.5 +/- 3.1 mug) and significantly reduced (P less than .05) in the E2-S group (309 +/- 49 mg and 5.2 +/- 0.1 mug) compared with those of either the O-S group or the E2-LHRH group. Thus LHRH treatment increased mean luteal weight and mean luteal progesterone content while E2 pre-treatment depressed the same parameters. These data suggest that pulsatile administration of synthetic LHRH is able to elevate serum LH levels to an extent sufficient to counteract both natural luteolysis and premature luteal regression induced by E2 treatment.