Effects of angiotensin converting enzyme inhibitor cilazapril and angiotensin II antagonist saralasin in ovarian hyperstimulation syndrome in the rabbit


SAHIN Y., Kontas O. , Muderris I. I. , CANKURTARAN M.

GYNECOLOGICAL ENDOCRINOLOGY, vol.11, no.4, pp.231-236, 1997 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 11 Issue: 4
  • Publication Date: 1997
  • Doi Number: 10.3109/09513599709152539
  • Title of Journal : GYNECOLOGICAL ENDOCRINOLOGY
  • Page Numbers: pp.231-236

Abstract

We investigated the possible effects of the angiotensin converting enzyme (A CE) inhibitor cilazapril and angiotensin II antagonist saralasin on ovulation, ovarian steroidogenesis and ascites formation in the ovarian hyperstimulation syndrome (OHSS) in the rabbit model. OHSS was induced in rabbits by human menopausal gonadotropin (hMG) and intermittent human chorionic gonadotropin (hCG). In the cilazapril group (n = 10), animals also received cilazapril 2 mg/kg intraperitoneally daily for 7 days. In the saralasin group (n = 8), animals received saralasin intraperitoneally 1 h before or 1 h after hCG administration. Control animals (n = 8) received intraperitoneal saline solution. Serial blood samples were drawn on days 1, 5, 7 and 9 to measure serum estradiol and progesterone levels. On day 9, all rabbits underwent surgical exploration. Peritoneal and pleural fluid formation, ovarian weights and number of ovulations were determined. The volume of the ascitic and pleural fluids after hyperstimulation were not statistically different between the control, cilazapril and saralasin groups. The weight gains and ovarian weights of animals were similar between treatment and control groups. Saralasin significantly (p < 0.05) inhibited ovulation, but cilazapril did not. Cilazapril and saralasin did not affect progesterone production. Only cilazapril significantly decreased estradiol production (p < 0.05). In conclusion, the ACE inhibitor cilazapril and angiotensin II antagonist saralasin did not prevent ascites formation in OHSS. The ovarian renin-angiotensin system may not be the only factor acting in ascites formation in the OHSS.