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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．
To observe the mechanism of vasoconstriction induced by hemolytic phosphatidylcholine (LPC) and the effect of vascular endothelium on vasoconstriction induced by LPC in isolated rabbit thoracic aorta rings. Preincubation of 10μmol·L-1 LPC for 30min significantly enhanced the contractile response of 5-HT to 5-HT in rabbit thoracic aortic rings and increased the peak tension induced by 0.1μmol·L-15-HT to about 2.5 Times, EC50 decreased, shrinkage curve shifted to the left. The PKC inhibitor staurosporine (100nmol·L-1) could inhibit the vasoconstriction of LPC and restore the EC50. The vascular endothelial cells were removed or 100μmol·L-1 L-monomethyl-arginine L-NMMA pretreatment can significantly enhance the vasoconstriction of LPC, L-NMMA stronger (P <0.001). The results suggest that LPC may promote 5-HT-mediated vasoconstriction through the PKC pathway, and vascular endothelial may play a regulatory role.