Three groups of 6 ewes were laparotomized on day 9 of an estrous cycle (estrus = day 0) and the corporà lutea (CL) were marked with India ink. Indwelling cannulae were inserted into the uterine horn adjacent to the CL in groups 2 and 3. Group 1 was injected intramuscularly (i.m.) with corn oil twice daily on day 9. Group 2 received 750 microng 17beta-estradiol (E2) i.m. twice daily on day 9 plus intrauterine injections of indomethacin (INDO) vehicle on days 9 through 13. Group 3 received in the same estrogen treatment plus the injection of 20 mg INDO twice daily on days 9 through 13. Jugular venous samples were taken once daily on days 9 through 14 for progesterone analysis. At re-laparotmy on day 14, the ovaries were examined for new ovulations, and the ovary bearing the marked CL was removed. Results showed that E2 induced premature luteal regression as indicated by decreased CL weights and plasma progesterone levels. INDO when given in conjunction with E2 effectively blocked the luteolytic action of E2. These results suggest that the luteolytic action of E2 is mediated via increased prostaglandin secretion and release from the uterus.
PIP: The effect of indomethacin (INDO) on estrogen-induced luteolysis in the ewe was studied. 3 groups of 6 ewes received laparotomy on Day 9 of the estrous cycle, and corpora lutea (CL) were marked with India ink. In Groups 2 and 3 the CL in the uterine horn adjacent to the existing CL were cannulated. Treatment was as follows: Group 1 served as the controls; Group 2 received 750 mcg of 17beta-estradiol (E2) twice daily on Day 9 plus intrauterine injectionsof the INDO vehicle twice daily on Days 9-13; Group 3 received treatment with E2 plus 20 mg INDO twice daily on Days 9-13. Serum progesterone was analyzed on Days 9-14. On Day 14, animals received a repeat laparotomy and ovaries were examined for new ovulations. The ovary bearing the marked CL was removed. Premature luteolysis was induced with E2 treatment as indicated by CL weights (mean 171 + or - 20 mg). INDO in conjunction with E2 treatment blocked this luteolytic effect (mean CL weights, 481 + or - 28 mg). This difference was significant (p less than .01). The pattern of progesterone results confirm the CL regression. Progesterone values for Group 2 were significantly decreased compared with Group 3 and with the controls. It is concluded that the luteolytic action of E2 is mediated via increased prostaglandin secretion and release from the uterus.