Effects of hyperoxia and hypoxia on vascular prostacyclin formation in vitro.
Effects of hyperoxia and hypoxia on vascular prostacyclin formation in vitro.
复制标题
高氧和低氧对体外血管前列环素形成的影响。
作者：
M. Stuart;Y. Setty;R. Walenga;J. Graeber;C. Ganley
暴露于高氧（O2）浓度，特别是在新生儿中，与以血管受累为特征的病理综合征（包括早产儿视网膜病变）的发展相关。观察到的一些初始血管变化似乎与前列环素形成的减少一致。人脐动脉暴露于氧气导致超过30%的抑制血管产生前列环素的能力，无论是从内源性储存的花生四烯酸或从外源性提供的基板。与此相反，缺氧（更接近胎儿环境）导致超过30%的刺激产生的前列环素从内源性或外源性花生四烯酸。当从处理的动脉节段制备微粒体时，这些影响持续存在。体外结果表明，新生儿分娩后暴露于O2可能会经历血管前列环素形成显着减少。抑制这种强效血管扩张剂和抗血栓代谢产物的产生可能在O2毒性的急性渗出期发挥重要作用。
Exposure to high oxygen (O2) concentrations, especially in the neonate, is associated with the development of pathologic syndromes characterized by vascular involvement including the retinopathy of prematurity. Some of the initial vascular changes observed appear consistent with a reduction in prostacyclin formation. Exposure of human umbilical arteries to oxygen resulted in more than 30% inhibition in the ability of the vessels to produce prostacyclin either from endogenous stores of arachidonic acid or from exogenously provided substrate. In contrast, hypoxia (which more closely approximates the fetal environment) resulted in more than 30% stimulation in the production of prostacyclin from either endogenous or exogenous arachidonic acid. When microsomes were prepared from treated arterial segments, these effects persisted. In vitro results suggest that neonates exposed to O2 after delivery may experience a marked decrease in vascular prostacyclin formation. Inhibition of the production of this potent vasodilator and antithrombotic metabolite could play an important role in the acute exudative phase of O2 toxicity.