The objective of this experiment was to determine the effects of controlled heat stress on ovarian function of lactating dairy cows. Estrus was synchronized (estrus = d 0), and cows were randomly assigned to either heat stress (n = 11; 29 degrees C, 60% relative humidity) or thermoneutral (n = 11; 19 degrees C, 60% relative humidity) treatment. For cows undergoing heat stress, ambient temperature (19 degrees C) was increased from d 11 to 13 of the estrous cycle (3.3 degrees C/d increase) and remained at 29 degrees C until d 21. Beginning on d 11, the growth and regression of ovarian follicles and corpora lutea were measured by using ultrasonography. Blood was collected daily by coccygeal venipuncture for measurement of serum concentrations of progesterone and estradiol. The second wave dominant follicle was more likely to ovulate in cows in the thermoneutral treatment than in cows undergoing heat stress (91 vs. 18% ovulation, respectively). Patterns of follicular growth in cows under-going heat stress were associated with decreased serum estradiol from d 11 to 21 and on the day of luteolysis. The average day of luteolysis was delayed by 9 d in heat-stressed cows. Conclusions were that follicular growth and development and luteolytic mechanisms were compromised in heat-stressed cows; as a result, luteolysis was delayed, and second wave dominant follicles did not ovulate.

The objective of this experiment was to determine the effects of controlled heat stress on ovarian function of dairy heifers. Estrus was synchronized in Holstein heifers (estrus = d 0), and heifers then were randomly assigned to either heat stress (n = 10; 33 degrees C, 60% relative humidity) or thermoneutral (n = 11; 21 degrees C, 60% relative humidity) treatment. For heat-stressed heifers, ambient temperature was increased from thermoneutrality to heat stress (33 degrees C) between d 9 and 14 (2.4 degrees C/d increase) after the synchronized estrus and remained between 31 and 33.5 degrees C until d 22. From d 11 to 21, the growth and regression of ovarian follicles and corpora lutea were measured by using ultrasonography, and blood was collected daily for serum progesterone and estradiol analyses. The second wave dominant follicle was larger for the heifers in the thermoneutral environment than for heat-stressed heifers, and ovulation of the second wave dominant follicle occurred in 9 of 11 thermoneutral heifers. For 6 of 10 heat-stressed heifers, the second wave dominant follicle regressed and was replaced by an ovulatory third wave dominant follicle. Smaller follicular size in heat stressed heifers was associated with decreased serum estradiol concentrations between d 11 and 21. Serum concentrations of progesterone during the luteal phase were similar, but luteolysis was delayed in heat-stressed heifers compared with onset in heifers in the thermoneutral treatment. Conclusions were that heat stress inhibited the growth and function of the dominant follicle so that most of the heat-stressed heifers had three follicular waves and a delay in corpus luteum regression.

Two trials were conducted to determine whether 7-d progestogen treatment beginning on d 17 of the estrous cycle altered 1) ovarian follicular development, 2) serum concentration of estradiol-17 beta (E2) and progesterone (P4), and 3) patterns of release of luteinizing hormone (LH). In both trials, Angus, Angus x Holstein, or Holstein cows 2 to 6 yr of age were randomly assigned to receive either melengestrol acetate (MGA, .5 mg.animal-1.d-1; n = 23), a progesterone-releaseing intravaginal device (PRID, n = 26) or to serve as untreated Controls (n = 14). Ultrasonography and blood sampling were performed daily throughout the experiment beginning on d 3 (Trial 1) or d 9 (Trial 2) of the estrous cycle. In Trial 2, blood samples were collected every 15-min for 6 h on d 17 (all cows) and d 20 and 23 (MGA and PRID cows) for determination of LH. Estrous cycle length was 3 to 5 d greater (P < .05) for MGA- and PRID-treated cows characterized by two (MGA-2 and PRID-2) or three (MGA-3 and PRID-3) dominant follicles than for control cows exhibiting two (Control-2) or three (Control-3) dominant follicles. A greater proportion (P < .05) of MGA- than of PRID-treated cows ovulated the follicle that was dominant at the beginning of treatment on d 17 (10 of 23 vs 1 of 26). Serum P4 concentrations declined 3 d earlier in Control-2 and MGA-2 cows than in Control-3, MGA-3 or PRID-3 cows.(ABSTRACT TRUNCATED AT 250 WORDS)

The objective of this study was to evaluate the timing of follicular waves in cows treated with bovine somatotropin (bST) by measuring ovarian responses to a luteolytic dose of PGF 2 alpha on d 12 of the estrous cycle. Thirty lactating cows (26 Holstein and 4 Guernsey) were assigned to receive bST (500 mg; n = 18) or saline (control; 1.5 ml; n = 12) every 14 d for three injection cycles. On d 12 of a synchronized estrous cycle, cows were injected with PGF 2 alpha to induce luteolysis. Following PGF 2 alpha, 9 cows ovulated from the dominant follicle during the first follicular wave (4 cows treated with bST and 5 control cows), and 14 cows ovulated from the dominant follicle during the second follicular wave (8 cows treated with bST and 6 control cows). Of the cows that ovulated during the second follicular wave, cows treated with bST had more class 3 follicles (> or = 10 mm) than did control cows. Concentrations of estradiol rose earlier after PGF 2 alpha injection in cows treated with bST than in control cows. This rise in estradiol was parallel to the development of dominant follicles. Serum concentrations of FSH were decreased in cows treated with bST. During the first and second estruses, equivalent numbers of cows treated with bST and control cows ovulated, but fewer cows treated with bST expressed estrus. These results are consistent with the hypothesis that cows treated with bST have reduced FSH, a faster turnover of dominant follicles, and differences in the timing of follicular waves. Treatment of cows with bST also increased the incidence of undetected estrus.