The endothelium-dependent effects of thimerosal on mouse pial arterioles in vivo: evidence for control of microvascular events by EDRF as well as prostaglandins.
The endothelium-dependent effects of thimerosal on mouse pial arterioles in vivo: evidence for control of microvascular events by EDRF as well as prostaglandins.
复制标题
硫柳汞对体内小鼠软脑膜小动脉的内皮依赖性作用：EDRF 和前列腺素控制微血管事件的证据。
DOI：
10.1038/jcbfm.1992.96
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Nelson,GH
中科院分区：
文献类型：
--
作者：
Rosenblum,WI;Nishimura,H;Ellis,EF;Nelson,GH
Thimerectin在体外引起内皮源性舒张因子（EDRF）和胰高血糖素从传导血管的合成和/或释放。我们使用活体显微技术测试了其对小鼠软脑膜小动脉的作用和作用机制。局部硫柳汞扩张软脑膜小动脉。激光/伊文思蓝技术产生的内皮损伤消除了这种影响。扩张也消除了局部l-NMMA，一种报道的EDRF合成抑制剂。局部硫柳汞还降低了在最小内皮损伤部位的血小板粘附/聚集（“捕获”）的发生率。通过l-NMMA预处理可以消除这种影响。硫柳汞扩张小动脉的能力不仅被认为消除EDRF合成/释放的治疗消除，而且被环氧合酶抑制剂消除。然而，抑制血小板粘附/聚集不受环氧合酶抑制的影响。硫柳汞显著增加了从关闭的颅窗恢复的前列腺素E2的产生。我们得出结论，硫柳汞对直径的扩张作用需要两种内皮源性药物：EDRF和一种或多种肾上腺素协同作用。然而，硫柳汞对局部血小板粘附/聚集的抑制作用似乎仅由损伤部位的EDRF增加引起。
Thimerosal causes synthesis and/or release of both endothelium-derived relaxing factor (EDRF) and prostaglandins from conductance vessels in vitro. We tested its effects and mechanism of action on mouse pial arterioles in vivo using intravital microscopic techniques. Topical thimerosal dilated pial arterioles. This effect was eliminated by endothelial injury produced by a laser/Evans blue technique. Dilation was also eliminated by topical l-NMMA, a reported inhibitor of EDRF synthesis. Topical thimerosal also reduced the incidence of platelet adhesion/aggregation (“capture”) at a site of minimal endothelial damage. This effect was eliminated by l-NMMA pretreatment. The ability of thimerosal to dilate arterioles was eliminated not only by treatments thought to eliminate synthesis/release of EDRF, but also by cyclooxygenase inhibitors. However, inhibition of platelet adhesion/aggregation was not affected by cyclooxygenase inhibition. Thimerosal significantly increased production of prostaglandin E2recovered from a closed cranial window. We conclude that the dilating effects of thimerosal on diameter require two endothelium-derived agents: EDRF and one or more prostaglandins acting in concert. However, the inhibiting effect of thimerosal on local platelet adhesion/aggregation appears to be caused only by an increase in EDRF at the injured site.