MELENGESTROL ACETATE AT GREATER DOSES THAN TYPICALLY USED FOR ESTROUSSYNCHRONY IN BOVINE FEMALES DOES NOT MIMIC ENDOGENOUS PROGESTERONE INREGULATION OF SECRETION OF LUTEINIZING-HORMONE AND 17-BETA-ESTRADIOL
Fn. Kojima et al., MELENGESTROL ACETATE AT GREATER DOSES THAN TYPICALLY USED FOR ESTROUSSYNCHRONY IN BOVINE FEMALES DOES NOT MIMIC ENDOGENOUS PROGESTERONE INREGULATION OF SECRETION OF LUTEINIZING-HORMONE AND 17-BETA-ESTRADIOL, Biology of reproduction, 52(2), 1995, pp. 455-463
Our working hypothesis was that doses of melengestrol acetate (MGA) gr
eater than those typically administered in estrous synchrony regimens
would regulate secretion of LH and 17 beta-estradiol (E(2)) as endogen
ous progesterone (P-4) does during the midluteal phase of the estrous
cycle. We also hypothesized that endogenous P-4 from the CL would inte
ract with MGA to further decrease the frequency of LH pulses and E(2).
Cows on Day 5 of their estrous cycle (Day 0 = estrus) were randomly a
ssigned to an untreated control group (CONT, n = 5) or to one of six M
GA treatment groups (n = 5 per group): 1) MGA administered orally each
day via a gelatin capsule at a dose of 0.5 mg MGA/cow with the CL pre
sent (0.5CL); 2) 0.5 mg MGA/cow daily in the absence of CL (0.5NO); 3)
1.0 mg MGA with CL present (1.0CL); 4) 1.0 mg MGA without CL (1.0NO);
5) 1.5 mg MGA with CL present (1.5CL); 6) 1.5 mg without CL (1.5NO).
MGA was administered for 10 days (Day 5 = initiation of treatment). To
regress CL, cows assigned to groups without CL received injections of
prostaglandin F-2 alpha (PGF(2 alpha;25 mg) on Days 6 and 7 of their
estrous cycle. Ah cows were administered PGF(2 alpha) at the end of th
e 10-day treatment period. During the treatment period, daily blood sa
mples were collected to determine concentrations of E(2). Serial blood
samples were collected at 15-min intervals for 24 h on Days 8, 11, an
d 14 to determine pattern of LH secretion. Frequency of LH pulses on D
ays 8, 11, and 14 was greater (p < 0.05) in cows without CL (0.5NO, 1.
0NO, and 1.5NO) than in cows with CL (0.5CL, 1.0CL, 1.5CL, and CONT).
Mean concentrations of LH were greater (p < 0.05) in cows from the 0.5
NO group on Days 8 and 11 and were greater (p < 0.05) in cows from the
0.5NO, 1.0NO, and 1.5NO groups on Day 14 as compared to cows with CL.
Overall mean concentrations of LH across Days 8, 11, and 14 were grea
test (p < 0.05) in cows from the 0.5NO group and were also greater (p
< 0.05) in cows from the 0.5NO, 1.0NO, and 1.5NO groups as compared to
cows in the 0.5CL, 1.0CL, 1.5CL, and CONT groups. Mean concentrations
of E(2) during the treatment period were greater (p < 0.05) in cows f
rom the 0.5NO group than in cows from either the 1.0NO or the 1.5NO gr
oup; these values were also greater (p < 0.05) in cows of the 0.5NO, 1
.0NO, and 1.5NO groups as compared to cows of the 1.0CL and CONT group
s. Therefore, we reject our working hypothesis because doses of MGA gr
eater than those typically used in estrous synchrony protocols did not
suppress LH and E(2) to the same extent that endogenous P-4 does. In
addition, MGA treatment when CL were present did not result in a furth
er suppression of LH pulse frequency or of E(2) as compared to the val
ues in control cows with functional CL.