【摘要】 在离体兔胸主动脉环模型上观察溶血性磷脂酰胆碱（ＬＰＣ）促血管收缩作用的机理以及血管内皮对ＬＰＣ促血管收缩作用的影响．１０μｍｏｌ·Ｌ－１ＬＰＣ预温育３０ｍｉｎ可显著增强兔胸主动脉环对５－羟色胺（５－ＨＴ）的收缩反应，使０．１μｍｏｌ·Ｌ－１５－ＨＴ诱导的峰值张力增加到约２．５倍，ＥＣ５０降低，收缩曲线左移．而蛋白激酶Ｃ（ＰＫＣ）抑制剂显形孢菌素（ｓｔａｕｒｏｓｐｏｒｉｎｅ，１００ｎｍｏｌ·Ｌ－１）能抑制ＬＰＣ的促血管收缩作用，ＥＣ５０恢复；去除血管内皮或加入１００μｍｏｌ·Ｌ－１左旋单甲基精氨酸（Ｌ－ＮＭＭＡ）预处理均可显著增强ＬＰＣ的促血管收缩作用，Ｌ－ＮＭＭＡ的作用更强（Ｐ＜０．００１）．结果提示，ＬＰＣ可能通过ＰＫＣ途径促进５－ＨＴ介导的血管收缩，血管内皮可能在其中起调控作用．更多还原

【Abstract】 The effect of lysophosphatidylcholine(LPC) on serotonin induced vascular contraction was investigated in the isolated rabbit thoracic aorta. Vascular contractions to serotonin were enhanced in the presence of LPC (10 μmol·L 1 ), a major component of oxidized low density lipoprotein (ox LDL). In the rings pretreated with LPC for 30 min, 0.1 μmol·L 1 serotonin elicited a 2.5 fold potent peak force compared with the controls. The concentration response curve shifted to the left with a lower EC 50 value. Staurosporine (100 nmol·L 1 ), an inhibitor of protein kinase C(PKC), prevented the procontractile effect of LPC. Denudation of endothelial cells and pretreatment with 100 μmol·L 1 N G monomethyl L arginine (L NMMA), an inhibitor of nitric oxide synthase, both potentiated the increased contractile response by LPC at the dose of 0.1 μmol·L 1 serotonin. L NMMA more potentially enhanced the effect than denudation of endothelial cells (P<0.001). The results suggest that LPC may exert a procontractile effect on blood vessels correlating with PKC, and that vascular endothelial cells may be involved in this event.更多还原