Severe leukocyte depletion does not affect follicular rupture in the rat.
This study was initiated in order to examine the involvement of leukocytes 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) administration, and ovarian content of neutrophils was estimated by assaying myeloperoxidase (MPO) activity. The stimulation of hCG increased ovarian MPO activity within 6 h (p < 0.01). Coadministration of inhibitors of eicosanoid synthesis into the ovarian bursa (0.5 mg/bursa) markedly augmented the action of hCG on ovarian MPO activity (p < 0.0001). To examine the possible participation of leukocytes in the process of follicular rupture, peripheral leukocytes were depleted by a single i.v. injection of vinblastine sulfate or cyclophosphamide 4 days before hCG treatment. In spite of a severe depletion in the number of circulating neutrophils or total leukocytes, ovulation rate remained normal. The hCG-stimulated increase in ovarian MPO activity reflects influx of neutrophils into the ovaries during the periovulatory period, and inhibitors of eicosanoid synthesis, which suppress ovulation, further enhance this 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 increase in ovarian neutrophil content. Likewise, severe depletion of peripheral neutrophil or total leukocyte counts did not prevent ovulation. The observed influx of neutrophils into the ovary seems to be a consequence of vascular changes associated with the ovulatory response, rather than an obligatory requirement for follicular rupture.
Chun
S Y
SY
Department of Hormone Research, Bernhard Zondek Hormone Research Laboratory, Weizmann Institute of Science, Rehovot, Israel.
Daphna-Iken
D
D
Calman
D
D
Tsafriri
A
A
D000818:Animals; D002452:Cell Count; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D006080:Ovarian Follicle / Q000187:drug effects / Q000502:physiology*; D010053:Ovary / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D010060:Ovulation / Q000187:drug effects / Q000502:physiology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012422:Rupture, Spontaneous; D014747:Vinblastine / Q000494:pharmacology
D006063:Chorionic Gonadotropin; D014747:Vinblastine; D003520:Cyclophosphamide; D009195:Peroxidase