THE EFFECT OF VOLATILE ANESTHETICS ON ENDOTHELIAL VASODILATION PROPERTY

本研究旨在阐明介导磷脂酶A2刺激的EDRF产生的信号转导，这是通过碱性释放EDRF控制内皮血管张力的主要机制之一，并研究挥发性麻醉剂对血管扩张现象的影响。本研究结果表明：(1)通过内皮细胞Ca2+/钙调素非依赖性一氧化氮合酶，A1F和钒酸盐介导的EDRF从内皮细胞释放直接或间接激活磷脂酶A2，其中环氧合酶和细胞色素P450介导的花生四烯酸代谢物可能起关键作用；(2)氟烷而非异氟烷或七氟烷抑制mellitin直接激活磷脂酶A2所刺激的松弛机制；(3)没有麻醉剂抑制G蛋白激活剂、A1F和钒酸盐间接激活磷脂酶A2所刺激的松弛机制。因此，本研究表明新的信号切断介导内皮磷脂酶a2诱导的EDRF产生，而氟烷的抑制作用不同于其他麻醉剂，在这一机制上。本研究的发现将取代药理学论文。

The current study was aimed to clarify the signal transduction mediating the phospholipase A2- stimulated EDRF production which is one of the major mechanism underlying endothelial vascular tone control via basally released EDRF and to examine the effects of volatile anesthetics on the vascular dilation phenomen.The results of the current study indicated that (1) activated phospholipase A2 directly by melittin or indirectly by A1F and vanadate mediated EDRF release from endothelium by means of endothelial Ca2+/Calmoduline-independent nitric oxide synthase, in which arachidonate metabolites by lypoxygenase and cytochrome P450 played possible crucial roles, (2) halothane but not isotlurane or sevoflurane inhibited this relaxation mechanism stimulated by direct activation of phospholipase A2 with mellitin and (3) no anesthetics inhibited this relaxation mechanism stimulated by indirect activation of phospholipase A2 with G protein activators, A1F and vanadate.Accordingly, the current study showed the novel signal prunsduction mediating endothelial phospholipase A2-induced EDRF production and inhibitory action of halothane, unlike other anesthetics, on this mechanism . The findings in the current study will be substituted to the pharmacological papers.