Literature DB >> 15019818

Gonadotropin-releasing hormone agonist administration reduced vascular endothelial growth factor (VEGF), VEGF receptors, and vascular permeability of the ovaries of hyperstimulated rats.

Yoshimitsu Kitajima1, Toshiaki Endo, Kengo Manase, Akira Nishikawa, Masabumi Shibuya, Ryuichi Kudo.   

Abstract

OBJECTIVE: Using hyperstimulated rats, to elucidate the mechanisms of gonadotropin-releasing hormone agonist (GnRH-a) treatment to prevent early ovarian hyperstimulation syndrome (OHSS).
DESIGN: Descriptive study of hyperstimulated rats as an early OHSS model with Western blot analysis, Northern blot hybridization, and vascular permeability assay.
SETTING: Experimental laboratory research. ANIMAL(S): Sprague-Dawley female rats were used for collecting ovarian samples. INTERVENTION(S): Hyperstimulated rats received consecutive GnRH-a treatment from the start of pregnant mare serum gonadotropin (PMSG) treatment through 2 days after hCG administration. MAIN OUTCOME MEASURE(S): Expressions of vascular endothelial growth factor (VEGF), VEGF receptor-1 (VEGFR-1: Flt-1), VEGF receptor-2 (VEGFR-2: KDR/Flk-1), and vascular permeability by Evans blue leakage. RESULT(S): GnRH-a treatment significantly reduced expressions of VEGF, VEGFR-1, and VEGFR-2 both in mRNA and protein levels in the ovaries of hyperstimulated rats. GnRH-a treatment also reduced vascular permeability in the ovaries of hyperstimulated rats. CONCLUSION(S): It is speculated that GnRH-a treatment may prevent early OHSS by reducing vascular permeability through the decrease in VEGF and its receptors.

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Year:  2004        PMID: 15019818     DOI: 10.1016/j.fertnstert.2003.11.012

Source DB:  PubMed          Journal:  Fertil Steril        ISSN: 0015-0282            Impact factor:   7.329


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