ABSTRACT
It is known that common symptoms of ovarian hyperstimulation syndrome (OHSS) such as ascites and anasarca are a consequence of the extravasation of fluid from leaky vessels into body cavities, where it accumulates. Due to this extravasation a deficit in circulating volume develops, which can lead to hemoconcentration and/or prerenal failure. It is clear that increased vascular permeability (iVP) after gonadotropin administration is the main factor causing OHSS, but as human chorionic gonadotropin (hCG) itself has no vasoactive properties, its actions must be mediated by other specific vasoactive factors. It is likely that hCG induces the release of one or several ovarian substances that have potent and direct systemic effects on the vascu lar system, and is therefore responsible for the pathophysiology and its clinical presentations1.
