THE EFFECT OF VOLATILE ANESTHETICS ON ENDOTHELIAL VASODILATION PROPERTY

本研究旨在阐明磷脂酶A2刺激的EDRF产生的信号转导机制，以及挥发性麻醉药对血管扩张现象的影响。本研究结果表明：(1)蜂毒素直接激活磷脂酶A2或A1F间接激活磷脂酶A2，钒酸通过内皮细胞钙/钙调素非依赖性一氧化氮合酶介导内皮释放EDRF，其中由溶氧合酶和细胞色素P450产生的花生四烯酸代谢产物可能在其中起关键作用。(2)氟烷而不是异氟烷或七氟烷可抑制蜂毒素直接激活磷脂酶A2所引起的这种松弛机制，以及(3)没有麻醉剂可抑制G蛋白激活剂A1F和钒酸间接激活磷脂酶A2所激活的这种松弛机制。因此，与其他麻醉药不同，本研究显示了一种新的信号转导途径，即介导内皮磷脂酶A2诱导的EDRF的产生和氟烷对这一机制的抑制作用。本研究中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.