Simple or repeated induction of superovulation: a study on ovulation rates and microvessel corrosion casts in ovaries of golden hamsters.

Repeatedly stimulated ovaries are reported to decrease the ovulation rate. One cause among others might be that the microvascular bed has been insufficiently developed. Therefore, 30-day-old golden hamsters were superovulated either once or repeatedly. At the light microscopic level, the ovulation rate in serially sectioned ovaries was indirectly determined by the occurrence of corpora lutea and of abnormal follicle rupture with oocyte release into the cortical stroma (IOR). For the study with scanning electron microscopy (SEM), the microvascular bed of the ovaries was cast with a polyester resin, and the corrosion casts of mature follicles observed. The histological sections of once-stimulated ovaries showed a large number of corpora lutea and IOR follicles. This indicated hyperovulation. In corrosion casts of once-stimulated ovaries, large-sized antral follicles with two layers of a dense capillary meshwork were observed. Capillary sprouts were aligned around the antrum 0 to 12 h after administration of human chorionic gonadotrophin (hCG), and these radiated towards the center of the antrum after 12 to 36 h had elapsed. The ovulation site was recognized at the follicle apex by three similarly sized structures which were either a sinusoid, an oocyte replica, or an opening. Repeatedly stimulated ovaries produced a low number of corpora lutea and almost no IOR follicles. This was judged as hypoovulation. The microvessels of mature follicles were reduced in number and incompletely cast. Widespread resin leakages were conspicuous in the follicle wall 36 h after hCG injection, but the capillary sprouts radiated towards the center of the antrum. No ovulation site was detectable. It is concluded, that capillary sprouts are induced before luteinization. The ovulation site is indicated by particular changes in its microvascular bed. An insufficiently developed microvascular bed may be responsible for hypoovulation in repeatedly stimulated ovaries.