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Submitted on June 10, 2005
Accepted on October 24, 2005
Departments of Obstetrics and Gynecology (T.E., K.N., T.H.) and Pathology (M.C., N.S.), Sapporo Medical University, School of Medicine, South 1 West 16 Chuo-ku, Sapporo 060-8556, Japan
* To whom correspondence should be addressed. E-mail: endot{at}sapmed.ac.jp.
We investigated the mechanism by which a GnRH agonist (GnRHa) affects ovarian vascularity, vascular permeability and expression of the tight junction protein claudin-5 in a rat model of ovarian hyperstimulation syndrome (OHSS). Hyperstimulated rats received excessive doses of PMSG (50 IU/day) for 4 consecutive days, from days 25 to 28 of life, followed by 25 IU of hCG on day 29. Control rats received 10 IU of PMSG on day 27 of life, followed by 10 IU of hCG on day 29. GnRHa (Leuprolide 100 µg/kg/day) was administered to some hyperstimulated rats either on days 29 and 30 (short-term GnRHa treatment) or from day 25 to day 30 (long-term GnRHa treatment). Ovarian vascular density (vessels/10 mm2) and vessel endothelial area (%) were assessed by immunohistochemical analysis of the distribution of von Willebrand factor, while vascular permeability was evaluated based on leakage of Evans blue. High doses of PMSG and hCG significantly increased ovarian weight, vascular permeability, vascular density and the vessel endothelial area, while significantly reducing expression of claudin-5 protein and mRNA. All of these effects were significantly and dose-dependently inhibited by administration of GnRHa. This suggests that reduced expression of claudin-5 plays a crucial role in the increased ovarian vascular permeability seen in OHSS and that its expression can be modulated by GnRHa treatment. Indeed, preventing redistribution of tight junction proteins in endothelial cells and the resultant loss of endothelial barrier architecture might be the key to protecting patients against massive extravascular fluid accumulation in cases of OHSS.
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