血脂康对家兔血管成形术后内膜增殖及内皮功能的影响(摘要)

Background Hyperhomocysteinemia (prevalent in rural northern China)is an emerging risk factor for arterial endothelial dysfunction in CAD, which can be improved with folic acid supplementation. Such homocysteine-lowerying dosage of folio acid ( ＜ 1 mg/d ) can reduce restenosis after PTCA, but not the cardiovascular events.Folic acid has additional vascular protection in antixidation, NO synthase protection, angiogenesis-promotion and cytokines reduction.

长期血糖控制可影响高血糖对1型糖尿病患者内皮功能的持续作用

1型糖尿病与大血管病变发病率增加有关,这部分是由于高血压和血脂异常等传统危险因素增加,但近年研究提示高血糖也有重要作用.

Angiotensin-converting enzyme 2 (ACE2)-angiotensin (1-7) [Ang (1-7)]-Mas constitutes the vasoprotective axis and is demon-strated to antagonize the vascular pathophysiological effects of the classical renin -angiotensin system .We hypothesize that upregulation of ACE2-Ang (1-7) signaling protects endothelial function through reducing oxidative stress , thus resulting in beneficial outcome in di-abetes.Ex vivo treatment with Ang (1-7) augmented endothelium-dependent relaxation (EDR) in renal arteries from diabetic patients . Both Ang (1-7) infusion via osmotic pump (500 ng? kg -1? min-1 ) for 2 weeks and exogenous ACE 2 overexpression mediated by ad-enoviral ACE2 via tail vein injection rescued the impaired EDR and flow-mediated dilatation ( FMD) in db/db mice.Diminazene acetu-rate treatment (15 mg? kg-1? d-1 ) activated ACE2, increased the circulating Ang (1-7) level, and augmented EDR and FMD in db/db mouse arteries.In addition, activation of the ACE2-Ang (1-7) axis reduced reactive oxygen species (ROS) overproduction de-termined by dihydroethidium staining , CM-H2DCFDA fluorescence imaging , and chemiluminescence assay in db/db mouse aortas and also in high-glucose-treated endothelial cells .Pharmacological benefits of ACE 2-Ang ( 1-7 ) upregulation on endothelial function were confirmed in ACE2 knockout mice both ex vivo and in vitro.We elucidate that the ACE2-Ang (1-7)-Mas axis serves as an important signal pathway in endothelial cell protection in diabetic mice , especially in diabetic human arteries .In summary, endogenous ACE2-Ang (1-7) activation or ACE2 overexpression preserves endothelial function in diabetic mice through increasing nitric oxide bioavail -ability and inhibiting oxidative stress , suggesting the therapeutic potential of ACE 2-Ang(1-7) axis activation against diabetic vasculop-athy.

高血压病患者肱动脉内皮功能与心脏舒张功能的超声研究

高血压病是常见的慢性病, 也是心脑血管病主要的危险因素. 本组应用超声检测高血压病患者肱动脉内皮功能、心脏超声评估左室舒张功能,同时通过评分法研究心脏左室舒张功能,探讨二者功能改变的相关性,以期为高血压病早期干预提供客观的影像学指标.

Objective:To study the hemodynamic condition of uterine artery and renal artery in preeclampsia patients and its relationship with endothelial function and invasive function. Methods:Preeclampsia puerperas were enrolled in observation group of the research, including 20 cases each with mild preeclampsia, moderate preeclampsia and severe preeclampsia; healthy puerperas were enrolled in control group. Then color Doppler ultrasound was used to detect hemodynamic parameters of uterine spiral artery and bilateral renal interlobar artery, enzyme-linked immunosorbent assay was used to detect endothelial function indexes in serum, and PCR was used to detect invasive function parameters in placenta.Results: S/D, PI and RI of uterine spiral artery and bilateral renal interlobar artery in mild, moderate and severe preeclampsia patients were all higher than those of control group; the more severe the preeclampsia condition was, the higher the S/D, PI and RI of uterine spiral artery and bilateral renal interlobar artery were; mRNA contents of Cst L, Cst D and MMP-9 in placenta of mild, moderate and severe preeclampsia patients were lower than those of control group, and mRNA contents of RECK as well as serum sFlt-1, sEng, AT1-AA and AngII contents were higher than those of control group; the more severe the disease degree was, the lower the mRNA contents of Cst L, Cst D, and MMP-9 were, the higher the mRNA contents of RECK as well as serum sFlt-1, sEng, AT1-AA and AngII contents were.Conclusion:Resistance of uterine artery and renal artery in preeclampsia patients increases, and it is closely related to endothelial dysfunction and invasive function loss.

Background: Ongoing low-grade inflammation and endothelial dysfunction persist in children with coronary lesions diagnosed with Kawasaki disease (KD). Statins, frequently used in the management of high cholesterol, have also shown to improve surrogate markers of infl ammation and endothelial dysfunction. This study was undertaken to investigate the effi cacy and safety of pravastatin in children with coronary artery aneurysms due to KD.
Methods: The study enrolled 14 healthy children and 13 male children, aged 2-10 years, with medium-to-giant coronary aneurysms for at least 12 months after the onset of KD. Pravastatin was given orally to the KD group at a dose of 5 mg/day for children under 5 and 10 mg/day for children older than 5 years. To determine the effects of pravastatin on endothelial function, high-frequency ultrasound was performed before the start of the study and 6 months after pravastatin therapy. The parameters measured were brachial artery flow-mediated dilation (FMD), non-flow mediated dilation (NMD), and carotid artery stiffness index (SI). High sensitive C-reactive protein (hs-CRP) levels, the circulating endothelial progenitor cells (EPCs) number, and serum lipid profiles were also determined at baseline and after 6 months of pravastatin treatment.
Results: Before treatment, the KD group had significantly decreased FMD (P<0.05) and increased SI and hs-CRP levels (P<0.05) compared with controls. After 6 months of pravastatin therapy, FMD improved significantly compared to the baseline KD group (3.16±6.49 to 10.05±7.74, P<0.05), but remained significantly less than that in the control group with no signifi cant changes in NMD and SI. There were signifi cant decreases in markers of inflammation after treatment. The hs-CRP levels decreased signifi cantly from 2.93±0.81 mmol/L to 2.14±0.82 mmol/L (P<0.05) and the serum apo-B and apo-B/apo-A1 ratio were also reduced (P<0.05) in the KD group. However, the circulating EPC number was not signifi cantly different between baseline and that following pravastatin treatment in the KD group and the control group (P>0.05). No signifi cant complications were noted with paravastatin therapy.
Conclusions: Pravastatin improves endothelial function and reduces low-grade chronic infl ammation in patients with coronary aneurysms due to KD. Children with coronary aneurysms due to KD may benefit from statin therapy.