Ovarian hyperstimulation syndrome-model rats; the manifestation and clinical implication

Ovarian hyperstimulation syndrome (OHSS) is the most serious complication of ovulation induction with the gonadotropins. Though vascular endothelial growth factor (VEGF) has been implicated as a prime causative factor of OHSS progression, other factors must also be involved in the pathogenesis of OHSS. We have established an experimental model of OHSS in immature female rats. The ovarian weights and vascular permeability of the OHSS model rats are significantly increased by the ovarian stimulation with human chorionic gonadotropin (hCG). hCG elicits VEGF production in OHSS model rat ovaries. The addition of potent synthetic progesterone antagonist RU486, which reduces the extension of OHSS, attenuates the ovarian kinin and VEGF production dose-dependently whereas the VEGF gene expression was stable. VEGF protein detected in both the lung and the liver of the OHSS model rats is not affected at 24 h after the addition of hCG and RU486 in contrast to the ovary. Our results demonstrate that progesterone is implicated in the development of OHSS, in part, to enhance the ovarian VEGF production by post-transcriptional and organ-specific control.