Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2004
Ex vivo reactivity of the ovarian vascular bed to noradrenaline and carbachol during ovarian hyperstimulation syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Oriowo M A
Аннотация
OBJECTIVE: To study reactivity of the ovarian vascular bed to noradrenaline and carbachol during an experimentally induced ovarian hyperstimulation syndrome (OHSS) in rabbits.
MATERIALS AND METHODS: Rabbits were treated with human menopausal gonadotropin (75 IU) daily for 6 days, followed by human chorionic gonadotropin (2,500 IU) to induce OHSS. The ovarian vascular bed was isolated and perfused with physiological solution and its reactivity to injected noradrenaline and acetylcholine was examined.
RESULTS: The mean weight of the hyperstimulated ovary was 2.85 +/- 0.5 g compared to 0.25 +/- 0.1 g for the control rabbits. There was no significant difference in (a) the basal perfusion pressure of the ovarian vascular bed ex vivo; (b) the potency of, or maximum response to, noradrenaline, and (c) agonist dissociation constant or receptor density. Carbachol induced significantly greater vasodilation in ovarian vascular beds from hormone-treated rabbits, indicating a greater role for nitric oxide in this syndrome, as further supported by the observation that NW-nitro-L-arginine methyl ester hydrochloride (L-NAME) was more effective against carbachol-induced response in hormone-treated rabbits.
CONCLUSION: In the rabbit model of OHSS, carbachol produced an increased ex vivo vascular response but noradrenaline did not.
MATERIALS AND METHODS: Rabbits were treated with human menopausal gonadotropin (75 IU) daily for 6 days, followed by human chorionic gonadotropin (2,500 IU) to induce OHSS. The ovarian vascular bed was isolated and perfused with physiological solution and its reactivity to injected noradrenaline and acetylcholine was examined.
RESULTS: The mean weight of the hyperstimulated ovary was 2.85 +/- 0.5 g compared to 0.25 +/- 0.1 g for the control rabbits. There was no significant difference in (a) the basal perfusion pressure of the ovarian vascular bed ex vivo; (b) the potency of, or maximum response to, noradrenaline, and (c) agonist dissociation constant or receptor density. Carbachol induced significantly greater vasodilation in ovarian vascular beds from hormone-treated rabbits, indicating a greater role for nitric oxide in this syndrome, as further supported by the observation that NW-nitro-L-arginine methyl ester hydrochloride (L-NAME) was more effective against carbachol-induced response in hormone-treated rabbits.
CONCLUSION: In the rabbit model of OHSS, carbachol produced an increased ex vivo vascular response but noradrenaline did not.