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Abstract
In the present study our aim was to test two hypotheses: 1) inhibition of preovulatory
phase progesterone action can inhibit or delay ovulation, and 2) inhibition of preovulatory
phase progesterone action can inhibit postovulatory phase endometrial receptivity
for blastocyst implantation. Female rhesus monkeys showing normal cycle lengths were
randomly assigned to two groups: group 1 (n = 5) and group 2 (n = 7). The pretreatment
cycles were monitored for ovulatory pattern and, in treatment cycles, females were
allowed to cohabit with males from cycle days 6 to 28; group 1 animals received vehicle
alone, and group 2 animals received mifepristone (RU486, subcutaneously), 1 mg/animal
3 consecutive cycle days (days 7, 8, and 9 for 26-day pretreatment cycle length; and
days 8, 9, and 10 for 28-day pretreatment cycle length). Follicular phase mifepristone
resulted in a delay of ovulation (p < 0.01) when compared with pooled data of pretreatment
and treatment cycles of group 1 and pretreatment cycles of group 2. Despite delay
of ovulation, there was only a 20% decrease in the incidence of pregnancy in group
2 as compared with that in group 1. However, a delay (p < 0.05) in the appearance
of CG was noted in follicular phase mifepristone-treated cycles as compared with control
treatment cycles. On the other hand, ovulation could not be detected in three monkeys
in group 2; and, of these, two cycles were extended, but all three cycles were negative
for CG. These results support earlier reports that follicular phase mifepristone can
inhibit or disrupt follicular maturation, and delay ovulation. However, follicular
phase mifepristone failed to inhibit implantation, because gonadal hormones, including
progesterone, resume normal functions once ovulation takes place.
Keywords
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Article info
Publication history
Accepted:
May 20,
1997
Received in revised form:
May 20,
1997
Received:
April 18,
1997
Identification
Copyright
© 1997 Published by Elsevier Inc.