代谢综合征患者颈总动脉扩张性、紧张度和僵硬度的检测

目的探讨代谢综合征患者颈总动脉扩张性、紧张度和僵硬度的变化。方法采用彩色多功能超声诊断仪对33例正常人、76例非代谢综合征患者和83例代谢综合征患者颈总动脉的收缩和舒张内径进行检测,并计算动脉的扩张性、紧张度和僵硬度。结果与对照组和非代谢综合征组比较,代谢综合征组患者颈总动脉扩张性、紧张度明显下降(P<0.01),僵硬度明显升高(P<0.01);平均内膜中层厚度增厚(P<0.01);等级相关分析发现,左、右颈总动脉的扩张性和紧张度与代谢综合征成分数目呈负相关(P<0.01),左、右颈总动脉的僵硬度与代谢综合征成分数目呈正相关(P<0.01)。结论代谢综合征患者颈动脉的弹性降低,动脉硬化加剧;颈动脉超声可以作为评价代谢综合征患者心血管病危险性的无创性方法。

血管紧张素Ⅱ与动脉粥样硬化形成的研究进展

血管紧张素Ⅱ与动脉粥样硬化的关系近年来引起越来越多的关注,本文将血管紧张素Ⅱ通过对血管内皮细胞、单核,巨噬细胞、平滑肌细胞、血管新生和脂质代谢的影响而参与动脉粥样硬化形成的研究进展予以综述。

卡托普利和缬沙坦对兔动脉粥样硬化斑块中血管紧张素Ⅱ及纤溶酶原激活物抑制剂1表达的影响

目的观察兔动脉粥样硬化斑块局部血管紧张素Ⅱ和纤溶酶原激活物抑制物1的表达水平,并观察卡托普利和缬沙坦对其的影响。方法雄性健康新西兰兔随机分为高脂饮食组、卡托普利组、缬沙坦组和正常对照组。饲养10周后,取动脉血用发色底物法测定血浆纤溶酶原激活物抑制物1活性,放射免疫法测定血浆血管紧张素Ⅱ含量;取主动脉组织作病理形态学观察,免疫组织化学方法观察动脉粥样硬化斑块中血管紧张素Ⅱ及纤溶酶原激活物抑制物1的表达。结果与正常对照组相比,高脂饮食组血浆血管紧张素Ⅱ含量显著增高(494.86±67.98 ng/L比44.21±18.34 ng/L,P<0.01),血浆纤溶酶原激活物抑制物1活性显著提高(9.38±1.55 kAU/L比6.67±0.47 kAU/L,P<0.01),动脉粥样硬化斑块中血管紧张素Ⅱ及纤溶酶原激活物抑制物1阳性表达显著增高(46.97%±14.32%比4.17%±1.01%和48.50%±13.46%比1.33%±0.52%,P<0.01);与高脂饮食组相比,卡托普利组和缬沙坦组血浆纤溶酶原激活物抑制物1活性明显降低(7.23±0.46 kAU/L和7.42±0.59 kAU/L比9.38±1.55 kAU/L,P<0.05),斑块中血管紧张素Ⅱ阳性表达显著降低(26.30%±5.00%和27.83%±7.30%比46.97%±14.32%,P<0.05),斑块中纤溶酶原激活物抑制物1阳性表达显著降低(20.37%±8.23%和22.50%±7.06%比48.50%±13.46%,P<0.05)。斑块中纤溶酶原激活物抑制物1表达与血管紧张素Ⅱ表达呈正相关(r=0.796,P<0.01)。结论在高脂饮食所致动脉粥样硬化斑块中血管紧张素Ⅱ和纤溶酶原激活物抑制物1的表达增加,且二者呈正相关;卡托普利和缬沙坦减轻动脉粥样硬化斑块中血管紧张素Ⅱ和纤溶酶原激活物抑制物1的表达。

高频超声对缺血性脑卒中患者颈总动脉与颈动脉窦部的对比研究

目的运用高频超声探讨缺血性脑卒中(CAT)患者颈总动脉(CCA)与颈动脉窦部(CB)血管结构、血流动力学及血管功能的差异。方法应用高频超声对40例缺血性脑卒中患者颈动脉CB和CCA不同部位进行观察,分别测量收缩期内径(Ds)、舒张期内径(Dd)、内中膜厚度(IMT)、收缩期峰值流速(PSV)、阻力指数(RI)等参数,计算血管扩张性、紧张度、僵硬度等指标。结果 CCA、CB两组间IMT、PSV、RI比较,CB较CCA的IMT增厚(P<0.05),CB较CCA的PSV降低(P<0.05),CB较CCA的RI降低(P<0.05)。CB的动脉扩张性和动脉紧张度明显小于CCA(P<0.01);而CB动脉僵硬度则明显大于CCA(P<0.01)。结论颈动脉IMT结合动脉紧张度、动脉扩张性、动脉僵硬度可全面反映脑梗死患者颈动脉血管结构和功能变化的特征,提供更全面信息。同时颈动脉CB较CCA是容易发生颈动脉硬化的部位,CB应该作为早期评价动脉硬化的重点观察部位。

Angiotensin-（1-7）： new perspectives in atherosclerosis treatment

Angiotensin （Ang）-（1-7） is recognized as a new bioactive peptide in renin-angiotensin system （RAS）. Ang-（1-7） is a counter-regulatory mediator of Ang-II which appears to be protective against cardiovascular disease. Recent studies have found that Ang-（1-7） played an important role in reducing smooth muscle cell proliferation and migration, improving endothelial function and regulating lipid metabolism, leading to inhibition of atherosclerotic lesions and increase of plaque stability. Although clinical application of Ang-（1-7） is restricted due to its pharmacokinetic properties, identification of stabilized compounds, including more stable analogues and specific delivery compounds, has enabled clinical application of Ang-（1-7）. In this review, we discussed recent findings concerning the biological role of Ang-（1-7） and related mechanism during atherosclerosis development. In addition, we highlighted the perspective to develop therapeutic strategies using Ang-（1-7） to treat atherosclerosis.

Suppression of angiotensin Ⅱ stimulated responses in aortic vascular smooth muscle cells of experimental cirrhotic rats

Functional responses to angiotensin Ⅱ (AT-Ⅱ) were determined in aortic vascular smooth muscle cells (VSMCs) from experimental cirrhotic rats. Our data showed that AT-Ⅱ-stimulated extracellular acidification rate (ECAR), which was measured by Cytosensor microphysiometry, was significantly reduced in the aortic VSMCs from the cirrhotic rats as compared to those from the control animals. The ability of AT-Ⅱ to promote formation of inositol phosphates, the second messenger produced by the activation of Gq-coupled receptors, was also considerably suppressed in the cirrhotic VSMCs. Furthermore, the maximal p42/44 MAPK phosphorylation stimulated by AT-Ⅱ was significantly reduced in the cirrhotic VSMCs in contrast to that in the normal VSMCs. Taken together, our data clearly demonstrated that the functional responses to AT-Ⅱ was severely suppressed in aortic VSMCs in cirrhosis, indicating the impairment of general Gq-coupled receptor signaling and subsequent biological function in the cirrhotic VSMCs.

Baicalein protects against the development of angiotensin II-induced abdominal aortic aneurysms by blocking JNK and p38 MAPK signaling

An abdominal aortic aneurysm(AAA) is a permanent, localized dilatation of the abdominal aorta. In western countries, the morbidity of AAA is approximately 8%. Currently, pharmacotherapies for AAA are limited. Here, we demonstrate that baicalein(BAI), the main component of the Chinese traditional drug "Huang Qin", attenuates the incidence and severity of AAA in Apoe儃/儃 mice infused with angiotensin II(AngII). Mechanically, BAI treatment decreases AngII-induced reactive oxygen species(ROS) production in the aortic wall. Moreover, BAI inhibits inflammatory cell accumulation in the aortas of mice infused with AngII. It also inhibits AngII-induced activation of matrix metalloproteinase 2(MMP-2) and MMP-9 to maintain elastin content in vivo. In addition, it blocks AngII cascade by downregulating angiotensin type 1 receptor(AT1R) and inhibiting mitogen-activated protein kinases(MAPKs). Taken together, our findings show that BAI is an effective agent for AAA prevention.

Induction of thoracic aortic dissection: a mini-review of β-aminopropionitrile-related mouse models

Thoracic aortic dissection(TAD)is one of the most lethal aortic diseases due to its acute onset,rapid progress,and high rate of aortic rupture.The pathogenesis of TAD is not completely understood.In this mini-review,we introduce three emerging experimental mouse TAD models usingβ-aminopropionitrile(BAPN)alone,BAPN for a prolonged duration(four weeks)and then with added infusion of angiotensinⅡ(AngⅡ),or co-administration of BAPN and AngⅡchronically.We aim to provide insights into appropriate application of these three mouse models,thereby enhancing the understanding of the molecular mechanisms of TAD.