Current Hyphotesis on Ovulation.

The above background information on ovulation, along with the current literature on this topic, serve as the basis for the following “working hypothesis” on the mechanism of mammalian ovulation: The ovulatory surge in LII (or, exogenous hCG) Initiates acute changes in steroid and eicosanoid metabolism in the granulosa cells of mature follicles. The ensuing increases in local prostaglandins, lipoxins, kinins, platelet-activating factor, VEG/PF, and other vasoactive agents collectively cause substantial dilatation of the capillaries in the theca interim of the follicle wall. This significant change in the capillaries of ovulatory follicles results in a 4-fold increase in the volume of the ovarian vascular compartment.

Concomitant with this hyperemic response, the permeability of the thecal capillaries increases to the extent that serum proteins are exuded into the interstitial spaces of the Ibilicle in a manner characteristic of inflamed tissues. Since blood serum is well known for its ability 10 activate fibroblasts, it can be predicted that the exuded serum stimulates the quiescent fibroblasts in the theca externa and tunica. albuginea of an ovulatory follicle and causes them to transform into proliferating cells.

The activated thecal
fibroblasts begin secreting a metalloproteinase (perhaps stromolysin-1, which is regulated by NGF) that. degrades the extracellular matrix of collagenous connective tissue in the follicle wall. Ultimately, the follicle wall loses its tensile strength and eventually ruptures under the force of a modest, but effective, intrafollicular pressure.