Hyperstimulation and a Gonadotropin-Releasing Hormone Agonist Modulate Ovarian Vascular Permeability by Altering Expression of the Tight Junction Protein Claudin-5

• DOI: 10.1210/en.2005-0700
• Publication Date: 2005-11-04T01:29:31Z
• Authors: Yoshimitsu Kitajima; Toshiaki Endo; Kunihiko Nagasawa; Kengo Manase; Hiroyuki Honnma; Tsuyoshi Baba; Takuhiro Hayashi; Hideki Chiba; Norimasa Sawada; Tsuyoshi Saito
• Keywords: Ovarian hyperstimulation syndrome; Vascular permeability; Evans Blue; Human chorionic gonadotropin; Claudin

We investigated the mechanism by which a GnRH agonist (GnRHa) affects ovarian vascularity, vascular permeability, and expression of tight junction protein claudin-5 in rat model hyperstimulation syndrome (OHSS). Hyperstimulated rats received excessive doses pregnant mare serum gonadotropin (PMSG; 50 IU/d) for 4 consecutive days, from d 25 to 28 life, followed IU human chorionic (hCG) on 29. Control 10 PMSG 27 hCG GnRHa (leuprolide 100 μg/kg·d) was administered some hyperstimulated either 29 30 (short-term treatment) or (long-term treatment). Ovarian density (vessels per mm2) vessel endothelial area (percent) were assessed immunohistochemical analysis distribution von Willebrand factor, whereas permeability evaluated based leakage Evans blue. High significantly increased weight, density, reduced mRNA. All these effects dose-dependently inhibited administration GnRHa. This suggests that plays crucial role seen OHSS its can be modulated treatment. Indeed, preventing redistribution proteins cells resultant loss barrier architecture might key protecting patients against massive extravascular fluid accumulation cases OHSS.