Prevention of ovarian hyperstimulation syndrome in a rat model: efficacy comparison between cabergoline and meloxicam

Abstract Objective. To compare the efficacy of cabergoline (Cb2) and meloxicam in curbing vascular endothelial growth factor (VEGF) expression and preventing ovarian hyperstimulation syndrome (OHSS). Design. Randomized controlled, animal study. Setting. Academic facility. Sample. We used a total of...

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Veröffentlicht in:Acta obstetricia et gynecologica Scandinavica 2010-05, Vol.89 (5), p.692-699
Hauptverfasser: Saylan, Arif, Arioz, Dagistan Tolga, Koken, Tulay, Dilek, Husniye, Saylan, Filiz, Yilmazer, Mehmet
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Sprache:eng
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Zusammenfassung:Abstract Objective. To compare the efficacy of cabergoline (Cb2) and meloxicam in curbing vascular endothelial growth factor (VEGF) expression and preventing ovarian hyperstimulation syndrome (OHSS). Design. Randomized controlled, animal study. Setting. Academic facility. Sample. We used a total of 50 immature Wistar female rats randomly to create an experimental OHSS model. Methods. Ten rats each formed the control group and mild OHSS group. The remaining 30 were separated into three equal groups of severe OHSS. Mild and severe OHSS were induced through ovarian stimulation with gonadotropins. One group with severe OHSS was administered a low-dose 100 μg/kg Cb2 therapy; another group with severe OHSS received 600 μg/kg meloxicam. Body weight, vascular permeability (VP), VEGF expression, ovary weight, and diameter were then compared. Main outcome measures. The efficacy of Cb2 and meloxicam for preventing OHSS. Results. Comparison of the severe OHSS groups with the controls and mild OHSS group revealed significant increases in VEGF expression, VP, ovary weight, and diameter. The increase in VEGF expression was demonstrated to be dependent on human chorionic gonadotropin doses. However, low-dose Cb2 and meloxicam therapies were shown to be ineffective in decreasing VEGF expression and VP, ovary weight, and ovary diameter in severe OHSS. Conclusions. VEGF elevation played a critical part in OHSS pathogenesis, but the therapies administered failed to curb VEGF expression.
ISSN:0001-6349
1600-0412
DOI:10.3109/00016341003592537