Dopamine (D) agonists (A) administration diminishes increased vascular permeability (iVP) in ovarian hyperstimulation syndrome (OHSS) animals by blocking vascular endothelial growth factor receptor 2 (VEGFR2) phosporylation (ph)

2004 ◽  
Vol 82 ◽  
pp. S309-S310
Author(s):  
R. Gomez ◽  
M. Gonzalez ◽  
J. Sanchez-Criado ◽  
C. Simon ◽  
J. Remohi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Permeability ◽  
Ovarian Hyperstimulation Syndrome ◽  
Growth Factor Receptor ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Ginkgo Biloba Extract 761 Reduces Vascular Permeability of the Ovary and Improves the Symptom of Ovarian Hyperstimulation Syndrome in a Rat Model

2021 ◽  
Author(s):  
Jie Zhang ◽  
Jie Huang ◽  
Xinhuan He ◽  
Ning Li ◽  
Yu Miao ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Treatment Group ◽  
Vascular Permeability ◽  
Chorionic Gonadotropin ◽  
Rat Model ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Abstract BackgroundGinkgo biloba extract (EGb) has been widely applied in the treatment of cerebrovascular and neurological diseases. However, the effect of EGb761 on ovarian hyperstimulation syndrome (OHSS), a vascular disorder and life-threatening complication of In vitro fertilization and Intracytoplasmic sperm injection therapy (IVF/ICSI), has not been evaluated. MethodsForty female Wistar rats aged 22-days old (D22) were divided into eight groups: Control rats received intraperitoneal injection of saline for 5 consecutive days (D22-D26); OHSS-model group received 10 IU equine chorionic gonadotropin (eCG) for 4 consecutive days (D22-D25) and 30 IU of human chorionic gonadotropin (hCG) on the 5th day (D26); Prophylactic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) one hour before injection of eCG (hCG) for 7 consecutive days; Therapeutic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) 48 hours after injection of eCG (hCG) for 7 consecutive days. ResultsWe found the therapeutic treatment group exhibited the lowest ovarian and renal mass index, vascular permeability, estradiol and progesterone concentrations, vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR) protein expression. ConclusionsEGb761 decreases vascular permeability in OHSS rat model by inhibiting VEGF and VEGFR expression, which may contribute to the prevention and treatment of OHSS. Furthermore, therapeutic medication is superior to prophylactic medication.

scholarly journals The kallikrein-kinin system, but not vascular endothelial growth factor, plays a role in the increased vascular permeability associated with ovarian hyperstimulation syndrome

1998 ◽  
Vol 20 (3) ◽  
pp. 363-374 ◽  
Author(s):  
H Kobayashi ◽  
Y Okada ◽  
T Asahina ◽  
J Gotoh ◽  
T Terao
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Ovarian Carcinoma ◽  
Vascular Permeability ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Kinin System ◽  
Kallikrein Kinin System ◽  
Endothelial Growth Factor

Ovarian hyperstimulation syndrome (OHSS) is a severe complication arising from controlled stimulation treatment. Vascular endothelial growth factor (VEGF) has recently emerged as an important factor which may be responsible for the hyperpermeability seen in OHSS. The purpose of the present study was to investigate and compare the mechanisms by which ascites in patients with OHSS and ovarian carcinoma induce increases in vascular permeability in an in vitro assay and an in vivo animal experiment. We found 8-fold lower VEGF levels in ascites from patients with OHSS than in those from patients with ovarian carcinoma. Although VEGF is produced by the ovaries, it is not necessarily the factor responsible for hyperpermeability. We also demonstrated that the vascular hyperpermeability produced by OHSS ascites was not abolished by specific neutralizing anti-VEGF antibodies, and that not all of the VEGF found in the ascites fluid is biologically active. Moreover, our results strongly suggest that the vascular permeability produced by OHSS ascites may depend on activation of the kallikrein-kinin system. Possible evidence for this phenomenon was obtained by demonstrating that the hyperpermeability caused by the ascites could be blocked by Trasylol (known to inhibit bradykinin synthesis) and potentiated by captopril (a kininase II inhibitor). Taken together, the results suggest that, although VEGF is found in ascites fluid from patients with OHSS, it is unlikely that the cause of OHSS involves VEGF production by the ovaries. The kallikrein-kinin system may be more important in the hyperpermeability seen in OHSS.

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