Ten normally cycling Hoi stein heifers were assigned to one of two environmental treatment groups (21.3 C, 59% RH or 32.0 C, 67% RH). PGF^^ was used to cause luteal regression and synchronize estrus. Least-squares analyses were conducted to characterize treatment, animal and withinanimal time trends in plasma progestins, estradiol, estrone, LH, prolactin and corticoids. Environmental treatment (32.0 C) evoked a 1.49 C increase in rectal temperature and a 3.59 C increase in skin temperatures. Length of estrus was shorter (P<.10) for the 32.0 C heifers. Two of four heifers at 21.3 C inseminated were pregnant at 40 days compared to none of five at 32.0 C. Average progestin concentration between treatments were not different (P>.10; .53 ng/ml at 21.3 C compared to .65 ng/ml at 32.0 C). Mean estradiol concentrations were significantly (P<.10) lower in 32.0 C heifers (3.45 pg/ml compared to 2.96 pg/ml). There was a significant elevation (P<.05) of estrone due to heat stress (1.55 pg/ml compared to 1.85). No significant differences (P>.10) were found in mean LH concentrations between heifers at 21.3 C or 32.0 C. Preovulatory peak LH concentrations were 32.2 and 33.2 ng/ml plasma, respectively. All animals had a preovulatory LH surge, suggesting that hyperthermia did not prevent the triggering mechanism for LH release. Mean prolactin (14.51 ng/ml at 21.3 C compared to 14.78 ng/ml at 32.0 C) and corticoid (8.01 ng/ml at 21.3 C compared to 7.76 ng/ml at 32.0 C) concentrations were not different between temperature treatments (P>.10). In an attempt to determine if plasma dilution may have occurred, total protein concentration and osmolality were measured. There v/as no difference (P>.10) in total protein concentration or osmolality between treatment groups. The affinity (K) of Cortisol for CBG was not a different between treatments (P>.10); however, the binding capacity of CBG for Cortisol was reduced (P<.05) in the 32.0 C heifers. Results of this experiment showed only subtle thermal effects on estradiol and estrone plasma concentrations and no effects on LH, progestins, corticoids and prolactin. Apart from possible hormonal involvement with duration of estrus, heat stress did not appear to affect the hormonal mileau in peripheral plasma associated with corpus luteum regression, follicle growth and ovulation. Eight days following ovulation in the last heifer, 200 ID ACTH was injected, IV, into the 10 heifers. The 32.0 C heifers responded with significantly lower (P<.10) corticoid concentrations. The 6th order regression response curves were not parallel (P<.01) suggesting that the hot group response was earlier to reach a peak (75 compared to 105 min.), had a lower magnitude (73.5 compared to 100.2 ng/ml corticoids) and was of shorter duration (4 compared to 5 hr.). Because the first experiment did not specifically consider environmental and hormonal effects on uterine temperature it was necessary to document possible estrogen induced uterine thermal changes. In the second experiment thermocouples were placed into the uterine serosa and saphenous artery of four dairy heifers. Injection of 3 mg estradiol-176 caused a .25 C decrease (P<.01) in the difference between uterine and aortic temperature (aT,) by 2,5 hr. postinjection. In contrast, there was no U~a significant change (P>.10) in the AT, after injection of saline. u~a The final experiment was an attempt to document and evaluate changes in uterine temperature during the period of luteal regression, follicle growth and ovulation induced by PGFp under conditions of a mild heat stress. Thermocouples were placed into the uterine serosa and aortic blood vessel of four dairy cattle. PGF^ caused an immediate drop in uterine and aortic temperatures, and a decrease in the AT of almost u-a .4 C at 45 min. postinjection. The two cows, in which thermocouples remained operational for the duration of the study, had monophasic daily uterine and aortic temperature rhythms. However, both temperatures lagged about 6 hr. behind air temperature changes. Uterine temperatures reached 40 C for periods of up to 6 hr. Failure to detect an association between AT and hormonal measurements may have been due to a time lag association. Not until the preovulatory surge of LH was there an appreciable rise in aT^_^ (P<.01), and this occurred at a time when estradiol was decreasing. The mild environmental heat stress may have contributed to the high uterine and aortic blood temperatures.