Phlebology · 2013
Cilostazol strengthens the endothelial barrier of postcapillary venules from the rat mesentery in situ.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sugiura Yasoo, Morikawa Takayuki, Takenouchi Toshiki, Suematsu Makoto, Kajimura Mayumi
Аннотация
OBJECTIVE: Although cilostazol, a phosphodiesterase 3 inhibitor, has been suggested to strengthen the endothelial barrier using cultured endothelial monolayers, its effect has not been tested in vivo. We, therefore, investigated effects of cilostazol on barrier properties of postcapillary venules of the rat in situ.
METHODS: Cilostazol was administered to the rats through oral gavage at 4 hours before the measurements. The hydraulic permeability (L(p)) and the effective osmotic pressure (σΔπ), molecular sieving properties of microvascular walls, were estimated in single mesenteric postcapillary venules by a micro-occlusion technique, first during control perfusion and then in the presence of histamine.
RESULTS: When the vessels were inflamed with histamine, cilostazol attenuated a transient increase in L(p) and prevented σΔπ from falling. Furthermore, it reduced baseline L(p) under a control state.
CONCLUSION: Cilostazol appears to tighten the endothelial barrier in situ, at least in part by inhibiting the cAMP-degrading enzyme in the endothelium.
METHODS: Cilostazol was administered to the rats through oral gavage at 4 hours before the measurements. The hydraulic permeability (L(p)) and the effective osmotic pressure (σΔπ), molecular sieving properties of microvascular walls, were estimated in single mesenteric postcapillary venules by a micro-occlusion technique, first during control perfusion and then in the presence of histamine.
RESULTS: When the vessels were inflamed with histamine, cilostazol attenuated a transient increase in L(p) and prevented σΔπ from falling. Furthermore, it reduced baseline L(p) under a control state.
CONCLUSION: Cilostazol appears to tighten the endothelial barrier in situ, at least in part by inhibiting the cAMP-degrading enzyme in the endothelium.