Anatomical considerations indicate that translocation of a serum protein to the follicular antrum requires its passage through the following structures: 1) the capillary endothelium of the ovarian vasculature, 2) the theca interna, 3) the basement membrane, and 4) the membrana granulosa. It is possible that selectivity and permeability properties of the barrier could reside within some or all of these layers.
It is tempting to suggest that initial permeability and selectivity of the blood-follicle barrier begins with the regulation of the ovarian vascular endothelial cells within the theca interna. One pathway implicated in the regulation of barrier permeability involves nitric oxide (NO; ). Binding of LH receptors stimulates endothelial nitric oxide synthase to synthesize NO. It has been suggested that NO, in turn, activates soluble guanylate cyclase (sGC; ). Once activated, sGC increases levels of cGMP to increase vasodilation, which results in increased barrier permeability. buy antibiotics online
Alternatively, the process of ovulation has been compared to an acute inflammatory response, evidenced by dramatic changes in the vasculature and edema of the follicles. The LH surge is responsible for an increased release of inflammatory agents (i.e., histamine, eicosanoids, and bradykinin), which results in an increase in ovarian blood flow that lasts for at least 9 h after the gonadotropic stimulation. Although an increased blood flow via inflammatory mediators and vascular endothelial growth factor has been suggested to increase vascular permeability, other mechanisms that specifically affect the endothelial cells may also be involved. For example, a negatively charged glycocalyx surrounding the endothelial cells as well as negatively charged serum proteins (i.e., albumin or orosomucoid) may create an electrostatic force that repels intermediate-size proteins with a net negative charge density.