INVOLVEMENT OF AN ACTIVATED POLYMORPHONUCLEAR IN CARDIOVASCULAR DISEASES

中性粒细胞（PMN）激活引起内皮细胞损伤的早期机制尚不清楚。特别是，一氧化氮和活性氧（ROS）的相互作用是未知的。本研究从内皮细胞的功能（肌松作用）出发，阐明细胞内外一氧化氮和活性氧在细胞损伤中的作用。1）在血管中加入活化的中性粒细胞，使血管平滑肌的舒张作用先有所减弱，然后逐渐恢复。这种现象可能是由一氧化氮和由PMN形成的ROS的相互作用引起的。2）过氧化氢（1mM）刺激内皮细胞中一氧化氮的形成。3）缺血再灌注时，血管舒张能力降低，再灌注后恢复到基础水平，提示血管张力的调节可能是通过NO和ROS的相互作用实现的。短期缺血后再灌注可引起舒张作用的暂时抑制。ROS损伤的早期阶段是静态的、可逆的。

Early step of mechanisms on endothelial cells injury caused by an activated polymorphonuclear (PMN) are not well understood. Especially, the interactions of nitric oxide and active oxygen species (ROS) are not known. In this study, we focused on the endothelial function (muscle relaxing action) to clarify the contribution of extra-and intracellular nitric oxide and ROS to cell injury.1) By the addition of activated PMN to blood vessel, at first the relaxation of blood muscle was a little reduced and then recovered gradually. This phenomena could be caused by the interaction of nitric oxide and ROS formed from PMN.2) Hydrogen peroxide (1 mM) stimulated a formation of nitric oxide in endothelial cells. Enhacement of NO formation lasted until cell death.3) During ischemia-reperfusion, the relaxing ability of blood vessel reduced at the moment and then return to the basal level following the reperfusion.From these results, the tonus of blood vessel could be regulated by the interaction of NO and ROS.In endothelial cells, the NO formation increased by exposing to ROS.Reperfusion after short term ischemia caused a temporal inhibition of relaxing action. Finally, the early step of ROS injury are static and reversible.