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Reproductive Sciences Program, Departments of Physiology (D.F.B., F.J.K.) and Biostatistics (M.B.B., N.E.C.), University of Michigan, Ann Arbor, Michigan 48109-0404
Address all correspondence and requests for reprints to: Dr. Fred J. Karsch, Reproductive Sciences Program, University of Michigan, 300 North Ingalls Building, Room 1101 SW, Ann Arbor, Michigan 48109-0404. E-mail: fjkarsch{at}umich.edu
Five experiments were conducted to test the hypothesis that PGs
mediate the endotoxin-induced inhibition of pulsatile GnRH and LH
secretion in the ewe. Our approach was to test whether the PG synthesis
inhibitor, flurbiprofen, could reverse the inhibitory effects of
endotoxin on pulsatile LH and GnRH secretion in ovariectomized ewes.
Exp 1–4 were cross-over experiments in which ewes received either
flurbiprofen or vehicle 2 weeks apart. Jugular blood samples were taken
for LH analysis throughout a 9-h experimental period. Depending on the
specific purpose of the experiment, flurbiprofen or vehicle was
administered after 3.5 h, followed by endotoxin, vehicle, or
ovarian steroids (estradiol plus progesterone) at 4 h. In Exp 1,
flurbiprofen reversed the endotoxin-induced suppression of mean serum
LH concentrations and the elevation of body temperature. In Exp 2,
flurbiprofen prevented the endotoxin-induced inhibition of pulsatile LH
secretion and stimulation of fever, reduced the stimulation of plasma
cortisol and progesterone, but did not affect the rise in circulating
tumor necrosis factor-
. In Exp 3, flurbiprofen in the absence of
endotoxin had no effect on pulsatile LH secretion. In Exp 4,
flurbiprofen failed to prevent suppression of pulsatile LH secretion
induced by luteal phase levels of the ovarian steroids progesterone and
estradiol, which produce a nonimmune suppression of gonadotropin
secretion. In Exp 5, flurbiprofen prevented the endotoxin-induced
inhibition of pulsatile GnRH release into pituitary portal blood. Our
finding that this PG synthesis inhibitor reverses the inhibitory effect
of endotoxin leads to the conclusion that PGs mediate the suppressive
effects of this immune/inflammatory challenge on pulsatile GnRH and LH
secretion.
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