高脂血症患者血流剪切率的变化及对血管功能的影响

目的：观察高脂血症患者血流剪切率的变化特点及探讨非诺贝特提高血管舒张功能的机制。方法:以20例正常人、62例高甘油三酯血症病人(其中30例予以饮食治疗、32例予非诺贝特治疗)为观察对象，以肱动脉B超测量血流、血管弹性和舒张功能等指标，检测血浆一氧化氮(NO)、氧化型低密度脂蛋白(Ox-LDL)、血脂的变化。结果:高甘油三酯血症病人超声显示平均血流剪切率（MSR）、血流介导的扩张效应(FMD)和血管弹性指标Da、Dr显著小于正常对照组，而平均血管壁紧张度(MCWT)显著大于正常对照组；血Ox-LDL浓度高于、NO水平低于正常对照组，且NO与MSR、 FMD水平呈正相关，与甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和Ox-LDL浓度呈负相关。8周的低脂饮食治疗可使TC、TG水平下降，但NO、Ox-LDL和血管超声指标未见显著改变；非诺贝特治疗组血管超声MSR 、FMD显著高于对照组，血TG、TC、LDL-C和Ox-LDL浓度低于、NO水平高于对照组。结论:高甘油三酯血症时MSR的下降和氧化因子Ox-LDL的升高共同参与内皮的损伤机制，导致NO水平下降，表现为血管舒张功能的下降和弹性下降，MSR的上升和Ox-LDL的下降有利于内皮功能的修复。

Change of shear stress in hypertriglycerlipidemic patients and the impact on endothelium-dependent relaxation

AIM: To investigate the profile of shear stress in hypertriglycerlipidemic patients and the impacts of fenofibrate on vascular endothelial function. METHODS: 62 hypertriglycerlipidemic patients were randomized into two groups (30 with low-fat diet treatment, 32 with fenofibrate) compared with 20 normal controls. Vessel structure, hemodynamic index and endothelium-dependent vasodilation of brachial artery were assessed by B-mode ultrasound imager. Serum NO, Ox-LDL, TC, TG, LDL-C, HDL-C were measured. RESULTS: Compared with controls, hypertriglycerlipidemic patients showed higher mean circumferential wall tension(MCWT) and lower mean shear rate(MSR), flow mediated dilatation(FMD) and Da, Dr. They had higher level of Ox-LDL and lower level of NO. NO was positive correlated with MSR, FMD and inversely correlated with TG, TC, LDL-C, Ox-LDL. 8 weeks of low-fat diet reduced TC and TG, but made no difference in NO, Ox-LDL and ultrasonic images. On the other hand, 8 weeks of fenofibrate treatment not only reduced TG, TC, LDL-C and Ox-LDL, but also elevated NO, MSR and FMD. CONCLUSION: The endothelial impairment of hypertriglycerlipidemic patients might be caused by lower level of MSR as well as oxidative substance such as Ox-LDL, which could inactivate NO and result in descent of endothelium-dependent relaxation. Elevation of MSR and elimination of Ox-LDL may improve endothelium-dependent relaxation.