SEVERE LEUKOCYTE DEPLETION DOES NOT AFFECT FOLLICULAR RUPTURE IN THE RAT

This study was initiated in order to examine the involvement of leukoc ytes in follicular rupture in the rat. To evaluate changes in ovarian neutrophil population, ovaries from eCG-primed (15 IU s.c. on Days 25- 26) rats were collected 0, 3, 6, and 9 h after hCG (4 IU) administrati on, and ovarian content of neutrophils was estimated by assaying myelo peroxidase (MPO) activity. The stimulation of hCG increased ovarian MP O activity within 6 h (p < 0.01). Coadministration of inhibitors of ei cosanoid synthesis into the ovarian bursa (0.5 mg/bursa) markedly augm ented the action of hCG on ovarian MPO activity (p < 0.0001). To exami ne the possible participation of leukocytes in the process of follicul ar rupture, peripheral leukocytes were depleted by a single i.v. injec tion of vinblastine sulfate or cyclophosphamide 4 days before hCG trea tment. In spite of a severe depletion in the number of circulating neu trophils or total leukocytes, ovulation rate remained normal. The hCG- stimulated increase in ovarian MPO activity reflects influx of neutrop hils into the ovaries during the periovulatory period, and inhibitors of eicosanoid synthesis, which suppress ovulation, further enhance thi s increase. Nevertheless, the periovulatory rise in ovarian neutrophil content does not seem to be obligatory for follicular rupture. Thus, inhibitors of eicosanoid synthesis block ovulation in the face of an i ncrease in ovarian neutrophil content. Likewise, severe depletion of p eripheral neutrophil or total leukocyte counts did not prevent ovulati on. The observed influx of neutrophils into the ovary seems to be a co nsequence of vascular changes associated with the ovulatory response, rather than an obligatory requirement for follicular rupture.