FOLLICULAR DEVELOPMENT, OOCYTE VIABILITY AND RECOVERY IN RELATION TO FOLLICULAR STEROIDS, PROLACTIN AND GLYCOSAMINOGLYCANS THROUGHOUT THE ESTROUS PERIOD IN SUPEROVULATED HEIFERS WITH A NORMAL LH SURGE, NO DETECTABLE LH SURGE, AND PROGESTIN INHIBITION OF LH SURGE
T. Wise et Rr. Maurer, FOLLICULAR DEVELOPMENT, OOCYTE VIABILITY AND RECOVERY IN RELATION TO FOLLICULAR STEROIDS, PROLACTIN AND GLYCOSAMINOGLYCANS THROUGHOUT THE ESTROUS PERIOD IN SUPEROVULATED HEIFERS WITH A NORMAL LH SURGE, NO DETECTABLE LH SURGE, AND PROGESTIN INHIBITION OF LH SURGE, Domestic animal endocrinology, 11(1), 1994, pp. 35-58
Estrous cycles of heifers (n = 137) were synchronized with prostagland
in (PGF(2 alpha)) and follicular development stimulated with follicle
stimulating hormone. Twenty-eight animals were administered Norgestome
t implants 12 hr prior to the initial PGF2 alpha injection to suppress
the LH surge that initiates ovulation. Animals were ovariectomized ev
ery 12 hr after the initial PGF2 alpha (7-9/time, 12-108 hr and at 199
and 240 hr post PGF2 alpha) and divided into three treatment groups t
o consist of: 1) animals exhibiting a normal luteinizing hormone (LH)
surge (n = 86), 2) animals in which no LH surge was detected (n = 23),
and 3) suppression of the LH surge via Norgestomet implants (72-108 h
r, n = 28). Follicular diameter was measured and follicular fluid was
collected for analysis of prolactin, estradiol, progesterone and glyco
saminoglycan concentrations. Progesterone concentrations were increase
d in animals exhibiting an LH surge as compared to animals in which no
LH surge was detected; primarily in large follicles (> 8 mm diameter)
after the LH surge. Animals not exhibiting an LH surge also had incre
ased follicular progesterone concentrations compared to Norgestomet-im
planted animals (242.3 +/- 36.3 vs 86.7 +/- 6.4 ng/ml, respectively, P
< .01), indicating some LH stimulation. Follicular estradiol in anima
ls exhibiting an LH surge increased up to the time of LH surge detecti
on and then declined whereas animals with no LH surge detected had fol
licular estradiol concentrations that declined after the PGF,OI inject
ion. No differences were noted between those that did not exhibit an L
H surge or in which the LH surge was suppressed with Norgestomet in re
lation to follicular estradiol concentrations. Follicular estradiol co
ncentrations increased with follicular size in all treatment groups (P
< .01). Follicular concentrations of prolactin were increased in smal
l follicles (P < .05; less than or equal to 4 mm diameter) and follicu
lar prolactin increased from 12 to 36 hr post PGF2 alpha injection, th
en declined after the LH surge. Follicular glycosaminoglycan concentra
tions decreased with increases in follicular size (P < .01) and were h
igher in animals that did not exhibit an LH surge (P < .01). No differ
ences in follicular glycosaminoglycans were noted between Norgestomet-
implanted animals and those not exhibiting an LH surge. In the animals
representing days 4 and 6 of the subsequent estrous cycle (192 and 24
0 hr post PGF2 alpha), numbers of small-sized follicles were increased
. Follicular progesterone and estradiol concentrations were related to
atretic large follicles unovulated from the prior estrus and a new wa
ve of growth in small and medium follicles. Follicular prolactin and g
lycosaminoglycans increased with time of the new estrous cycle and wer
e increased in smaller follicles (P < .01). Suppression of LH with pro
gestin implants (Norgestomet) may relate to early effects of progester
one, which may not be totally eliminated at target tissues and subsequ
ently alters the LH surge, steroidogenesis of the follicle, and ovulat
ion. Oocytes were predominantly found in the follicular fluid from ani
mals in which an LH surge was detected and in the buffer wash of folli
cles in which no LH surge was detected. Oocyte viability was higher in
animals exhibiting an LH surge (75% viable) whereas the oocytes of No
rgestomet-implanted animals were 75% degenerate.