Ca2+与NO在过氧化氢所致正常成年大鼠肠系膜微血管通透性增高中的作用

 目的 观察内皮细胞Ca2+浓度及NO生成在过氧化氢所致正常成年大鼠肠系膜微血管通透性增高中的作用。方法 通过测定在体大鼠肠系膜微血管静水传导性观察微血管通透性变化。采用钙荧光指示剂(Fura 2-AM)、NO荧光指示剂(DAF-2 DA)标记在体微血管内皮细胞，并应用荧光显微镜检测细胞内钙或NO的荧光信号，观察H2O2作用下内皮细胞内钙离子浓度([Ca2+]i)、NO的变化。结果 H2O2可增加正常成年大鼠微血管通透性（正常对照的6.13±0.87倍，P<0.01），同时增加微血管内皮细胞[Ca2+]i（714.58±144.70 nmol/L，P<0.01），并促进内皮细胞NO的生成（正常对照荧光强度的1034.3%±44.3%，P<0.01）。Ca2+通道阻滞剂氯化镧可抑制H2O2所引起的微血管通透性增加（P<0.01）及内皮细胞[Ca2+]i升高（P<0.01）。NOS抑制剂AP-Cav-1可抑制H2O2所引起的微血管通透性增加（P<0.01），但对H2O2的Ca2+增加作用无影响。结论 H2O2所致的通透性增加与细胞内Ca2+增加、NO的产生增多有关。

Effects of Ca2+ and NO on increased mesenteric microvessel permeability induced by H2O2 in rats

Objective To study the effect of endothelial [Ca2+]i and NO production on H2O2 induced mcrement of mesenteric microvessel permeability in normal adult rats.Methods Microvessel permeability was assessed by measuring hydraulic conductivity(Lp).H2O2-induced changes in endothelial [Ca2+]i and NO production were measured in Fura-2 AM(Ca2+fluorescent indicator) or DAF-2 DA(NO fluorescent indicator) loaded microvessels in vivo via fluorescence microscopy.Results H2O2 can increase mesenteric microvessel permability(6.13±0.87 times control value,P<0.01),endothelial [Ca2+]i [(714.58±144.70) nmol/L,P <0.01]and NO production(1034.3%±44.3% of control fluorescence intensity,P<0.01) in normal adult rats.Calcium channel blocker,Lanthanum Chloride(LaCl 3),inhibited the increase in microvessel permeability(P<0.01) and endothelial [Ca2+]i(P<0.01) induced by H2O2.NOS inhibitor,AP-Cav-1,can inhibit the increased microvessel permeability induced by H2O2 (P<0.01),but have no effect on increased endothelial [Ca2+]i.Conclusions Increased microvessel endothelial [Ca2+]i and NO production is involved in H2O2 induced increment of microvessel permeability.