大鼠动脉硬化闭塞模型两种构建方法的比较

背景：由于动脉硬化闭塞症的发病机制还不明确，所以建立动脉硬化闭塞症的病理动物模型，对于探明动脉硬化闭塞症的病因、病理生理、发病机制及防治药物的研究与开发均具有重要的意义。 目的：比较单纯高脂饲料喂养及给予内膜损伤加高脂饲料喂养大鼠动脉硬化闭塞模型复制建立的方法。 设计、时间及地点：随机对照动物实验，2007-08/2008-03于中国医科大学实验动物中心完成。 材料：清洁级3.0~4.0月龄健康纯种Wistar雄性大白鼠60只，体质量200 g。高脂饲料:62.8%基础饲料+20%猪油+150 g/L胆固醇+20 g/L胆酸钠+2 g/L丙基硫氧嘧啶。 方法：将60只大鼠随机分成3组，每组20只。普通饲养组给予普通饲料喂养；高脂饲养组给予高脂饲料喂养；高脂饲养加内膜损伤组给予内膜损伤加高脂饲料喂养。后两组同时给予维生素D3，30万u/kg体质量，右后肢肌肉注射,1次/月。 主要观察指标：①于内膜损伤后术后30 d，各组大鼠取血检测血浆总胆固醇、三酰甘油、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇浓度变化。②于内膜损伤后术后7，30，90 d时，取大鼠左后肢股-腘动脉，行苏木精-伊红等染色，光镜下观察股-腘动脉的病理变化。 结果：高脂饮食组大鼠与正常饮食组大鼠相比，高脂饮食组大鼠血清胆固醇 ，三酰甘油和低密度脂蛋白胆固醇均明显升高。病理显示：7 d高脂饲养组内皮细胞少量脱落，高脂饲养加内膜损伤组内皮细胞完全脱落、弹力板松弛，平滑肌细胞排列紊乱。90 d高脂饲养组内皮细胞完全脱落、平滑肌和胶原纤维增多、增厚，为早期硬化改变。高脂饲养加内膜损伤组内膜增厚、大量吞噬脂质、类脂质细胞、管腔闭塞。 结论：单纯给予大鼠高脂、高胆固醇饲料喂养不易形成动脉硬化闭塞症病变，大鼠股-腘动脉内注入蒸馏水损伤内皮加高脂饲料喂养可较快形成与人动脉硬化闭塞症相似的、较成熟的大鼠动脉硬化闭塞模型。     

加味补阳还五汤对兔髂动脉球囊损伤血管狭窄和氧化应激的影响

背景：近年研究证明,补阳还五汤具有扩张血管、改善微循环、抗炎、抗氧化应激和保护血管内皮细胞的功能,但其具体机制尚不清楚,尤其是对经皮腔内冠状动脉成形后再狭窄形成过程有何影响,目前很少见报道。 目的：观察加味补阳还五汤对兔髂动脉球囊损伤后血管狭窄及氧化应激的影响。 方法：将新西兰兔以随机抽签法分为对照组、模型组和药物组。对照组给予普通饲料,模型组、药物组给予高脂饮食。饲养2周后,模型组、药物组行髂动脉内膜剥脱术,对照组兔行假手术对照,药物组术后饲料中添加加味补阳还五汤药颗粒 2 mL/(kg•d),对照组及模型组喂食同前。4周后光镜观察兔髂动脉内膜的损伤情况,并检测血脂水平、血清超氧化物歧化酶活性和丙二醛水平的变化。 结果与结论：对照组髂动脉内膜薄且结构完整,无动脉硬化斑块;模型组内膜增厚,管腔明显狭窄,可见明显动脉粥样硬化斑块;药物组动脉粥样硬化斑块厚度减小,管腔狭窄程度较轻。药物组兔血清总胆固醇、三酰甘油和低密度脂蛋白胆固醇、丙二醛水平明显低于模型组,而高密度脂蛋白胆固醇、血清超氧化物歧化酶水平明显高于模型组(P < 0.05)。结果说明加味补阳还五汤具有较好的防止家兔球囊扩张损伤髂动脉所致的管腔狭窄及抗实验性动脉粥样硬化作用,其机制可能与其清除氧自由基抗氧化应激、调节脂质代谢等作用有关。     

蛋白酶体抑制剂MG132对动脉粥样硬化的影响

目的观察蛋白酶体抑制剂MG132对动脉粥样硬化的影响。方法将新西兰白兔30只随机分成高脂组、MG132(1)组和MG132(2)组。3组兔普通饲料喂养1w后行颈动脉球囊损伤术,术后高脂饲料(含1%胆固醇、3%猪油和15%蛋黄)喂养;MG132(1)组在术后高脂饲料喂养的同时血管局部应用蛋白酶体抑制剂MG132;MG132(2)组在术后高脂饲料喂养4w后血管局部应用蛋白酶体抑制剂MG132;3组均喂养8w后取颈总动脉血管制成病理切片行HE染色。结果高脂组兔的右颈总动脉管壁呈动脉粥样硬化改变。MG132(1)组兔右颈动脉血管组织结构基本正常。MG132(2)组兔的右颈总动脉管腔介于二者之间。结论局部应用蛋白酶体抑制剂MG132能够抑制血管内膜增生及动脉粥样形成,同时可能具有稳定斑块的作用。     

自制α-硫辛酸缓释片对氧化低密度脂蛋白致兔实验性动脉粥样硬化的影响

背景：由于硫酸锌半衰期短,必须多次给药,所以临床常用针剂剂型患者依从性差。 目的：利用食饵性兔动脉粥样硬化模型观察自制α-硫辛酸口服缓释片对动脉粥样硬化的预防作用及其可能途径。 设计、时间及地点：随机对照动物实验,于2008-05/09在南方医科大学珠江医院中心实验室完成。 材料：24只新西兰大白兔喂养1周后随机分成3组,分别为正常组、模型组、硫辛酸组,每组8只。 方法：正常组喂饲普通颗粒饲料。模型组用高脂饲料喂养,即在普通饲料中加入1 g胆固醇和8 g猪油。硫辛酸组用高脂饲料喂养,另外每只兔通过胃管给予自制硫辛酸缓释片300 mg/d。喂饲高脂饲料及预防性用药12周。 主要观察指标：实验结束后分别检测各组血清三酰甘油、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、丙二醛、超氧化物歧化酶、氧化低密度脂蛋白、一氧化氮及内皮素1水平。 结果：①纳入24只兔全部进入结果分析,无脱失。②喂饲高脂饲料后,模型组血清中总胆固醇、三酰甘油、低密度脂蛋白胆固醇、丙二醛、氧化低密度脂蛋白及内皮素1水平均显著高于正常对照组(P < 0.05), 高密度脂蛋白胆固醇、超氧化物歧化酶及一氧化氮水平显著低于正常对照组(P < 0.05)。③硫辛酸组血清中总胆固醇、三酰甘油、低密度脂蛋白胆固醇、丙二醛、氧化低密度脂蛋白及内皮素1水平均显著低于模型组(P < 0.05)。硫辛酸组超氧化物歧化酶及一氧化氮水平高于模型组(P < 0.01)。 结论：自制α-硫辛酸缓释片具有预防动脉粥样硬化的作用,其机制可能与其清除超氧阴离子等自由基,减轻氧化低密度脂蛋白对血管内皮细胞的氧化损伤有关。     

大鼠颈动脉粥样硬化性狭窄模型的建立

目的 建立一种经济实用、稳定、可靠的颈动脉粥样硬化动物模型.方法 SD大鼠分为3组,每组20只.采用球囊损伤法造成颈动脉内膜损伤后,分别给予普通饲料喂养,高脂饲料灌胃,同时给予腹腔注射维生素D,于第1,2,3,4周取出损伤侧血管,行HE染色,计算各组大鼠颈动脉狭窄率和内、中膜面积.结果 注射维生素D组大鼠颈动脉损伤处,第1周时内皮下即有泡沫细胞出现,随着时间延长逐渐出现内皮细胞脱落,内膜下泡沫细胞逐渐增多,血管平滑肌细胞增生,排列紊乱,至第4周时形成明显的动脉粥样斑块,管腔狭窄,较其他组差异有统计学意义(P＜0.05).结论 SD大鼠经球囊损伤颈动脉内膜后,结合高脂饲料及维生素D腹腔注射,可形成明显的颈动脉粥样硬化斑块,该方法时间短、操作简单、成功率高,可作为脑缺血性疾病研究的动物模型.     

家兔不同类型颈动脉斑块中基质金属蛋白酶-2表达的形态学研究

目的 建立不同类型颈动脉斑块的动物模型，比较不同斑块内基质金属蛋白酶-2（MMP-2）的阳性表达，观察MMP-2与斑块易损性的关系。方法 将动物随机分为高脂饲料（加或不加蛋氨酸）喂养组（B／A组），再以加或不加内膜空气干燥法分为B1、A1／B2、A2组，建立不同类型的颈动脉粥样硬化斑块的动物模型；免疫组化观察斑块内MMP-2表达，并进行纤维帽厚度／脂质核比值及免疫灰度测定。结果（1）病变管腔偏心性狭窄，呈不规则裂隙状；内膜不均匀增厚；中膜变薄；内、中膜大部分离。可见泡沫细胞的典型聚集形态和典型的纤维帽形态。（2）斑块易损性分析，依次是B1〉A1〉B2〉A2（P〈0．01）。（3）颈动脉斑块内MMP-2的阳性表达与斑块易损性呈正相关，免疫灰度依次是B1〉A1〉B2〉A2（P〈0．01）。结论 （1）采用高脂饲料加空气干燥法能成功建立颈动脉斑块的动物模型。（2）MMP-2的阳性表达与斑块的易损性呈正相关，MMP-2阳性表达结合纤维帽厚度／脂质核比值来判断颈动脉斑块易损性的方法能为研究斑块易损性提供一个有意义的标准。     

瑞舒伐他汀逆转动脉粥样硬化斑块及其与斑块稳定性的实验研究

目的 探讨动脉粥样硬化斑块发生、发展和破裂机制,以及瑞舒伐他汀对动脉粥样硬化斑块及其稳定性的影响.方法 18只普通健康大耳白兔随机分为对照组(6只)、高脂组(6只)和瑞舒伐他汀干预治疗组(6只).建立动脉粥样硬化动物模型.分别采用酶比色法、氧化酶终点法检测血清甘油三脂(TG)、总胆固醇(TC)、高密度脂蛋白-胆固醇(HDL-C)和低密度脂蛋白-胆固醇(LDL-C)水平;双抗体夹心酶联免疫吸附(ELISA)法、HE染色和免疫组织化学染色检测血清白细胞介素-6(IL-6)和热休克蛋白60(hsp60)表达水平;图像分析软件计算血管面积、斑块面积、斑块比例及hsp60阳性表达面积.结果 至实验结束时,瑞舒伐他汀干预治疗组动物血清甘油三脂、总胆固醇和低密度脂蛋白-胆固醇水平以及IL-6和hsp60表达水平均低于高脂组(P相似文献   

颈动脉粥样硬化性狭窄动物模型的建立

目的 探讨建立经济实用、稳定可靠的适于颈动脉粥样硬化性狭窄(CASS)外科治疗研究的CASS动物模型的条件。方法 新西兰白兔25只，采用血管内膜气体干燥损伤法在动物的颈总动脉上造成特定条件的损伤，然后以特定高脂饲料喂养动物不同时间。评价各组动物血管狭窄程度和病理改变特点。结果 1月组、2月组和3月组各组中重度狭窄均达到80％。病理检查证实高脂喂养2个月时，动脉的粥样硬化病理改变已属于较成熟的纤维斑块期。结论 按本实验方法，损伤后喂养2个月的动物颈动脉狭窄程度和病理改变程度皆符合CASS外科治疗之实验研究需要。     

高脂喂养加干燥气体损伤构建颈动脉狭窄动物模型

目的探讨建立经济实用、稳定可靠的适合颈动脉粥样硬化性狭窄外科治疗研究的动物模型的条件。方法日本大耳白兔40只,采用血管内膜气体干燥损伤法在动物的颈总动脉上造成特定条件的损伤(160ml/min×15min),然后以特定高胆固醇饲料(饲料中含2%的胆固醇和6%的花生油)喂养动物不同时间(30天,60天和90天)。通过血脂测定、DSA、HE染色方法评价各组动物血管狭窄程度,再观察其病理改变特点。结果病理检查证实:随着喂养时间的延长,动脉粥样硬化程度在加重,高脂喂养加干燥气体损伤90天时,血管狭窄率达71.53±3.65%,动脉的粥样硬化病理改变已属十较成熟的粥样斑块期。结论按本实验方法,90天时颈动脉狭窄程度和病理改变程度符合颈动脉粥样硬化性狭窄外科治疗之实验研究需要。     

阿托伐他汀对动脉粥样硬化性脑梗死患者的调脂效果及颈动脉粥样硬化斑块的影响

目的分析阿托伐他汀对动脉粥样硬化性脑梗死患者的调脂效果及对颈动脉粥样硬化斑块的影响。方法 92例动脉粥样硬化性脑梗死患者采用随机数字表法随机分为阿托伐他汀(20 mg/d)治疗组和非他汀类药物治疗组(对照组),评价两组患者治疗前后血脂水平和颈动脉斑块变化。结果经阿托伐他汀治疗后,阿托伐他汀组患者血清总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平降低(均P0.05),高密度脂蛋白胆固醇水平升高(P0.05);颈动脉斑块面积、斑块厚度和颈动脉内-中膜厚度明显改善(均P0.05)。结论阿托伐他汀具有改善动脉粥样硬化性脑梗死患者血脂水平、软化甚至缩小颈动脉斑块作用,有利于脑梗死患者的二级预防且无明显不良反应。     

Effects of antithrombotic drug, Y-20811 on mural thrombus formation and intimal thickening following intimal injury.

Inhibitory effect of Y-20811 on platelet thrombus formation induced by mechanical intimal injury and subsequent intimal fibrous thickening was studied. In the short term experiment, polyethylene tubing was inserted into the rabbit aorta and was drawn out one hour after with or without Y-20811 administration, then the rabbits were sacrificed. In the experiment for the quantitative analysis of platelet adhesion, 51Cr-labeled platelets were used. Radioactivities of 2cm length of the injured segment of the thoracic aorta and the proximal 2cm of the normal segment were measured. Radioactivity of the injured segment was significantly lower in rabbits treated with Y-20811 than the control ones. The mean thickness (area of thrombi/length of injured intima) and the maximal thickness of the mural thrombi in the Y-20811-treated rabbits were significantly lower than those in control rabbits. De-endothelialized area showed raised platelet thrombi in the control group and diffuse thin-layered platelet sheets in Y-20811-treated rabbits. In the long term experiment, polyethylene tubing was indwelled for 24 hours. Rabbits were sacrificed 10 days after drawing out the tubing. Through the experiment Y-20811 was injected intravenously every 24 hours. There was no significant difference between the control group and the Y-20811-treated one in both mean thickness and maximal thickness of the intimal fibromuscular thickening. The experiments indicate that Y-20811 has an inhibitory effect on platelet thrombus formation following intimal injury, but subsequent myointimal thickening is not inhibited by the drug.     

MRI characterization of atherosclerotic arteries: diagnosis of plaque rupture

Plaque stability and its counterpart, vulnerability, depend on the relative amount and morphology of its principal components: lipid core and fibrous cap. Lipids are mainly made of cholesterol esters and cholesterol monohydrates, but phospholipids and triglycerides are also present. Major chemokines, cytokines, enzymes and markers of inflammation are locally produced, which interact and degrade the arterial matrix, but also stimulate smooth muscle cells and osteopontine production. Due to these differences in composition, the lipid cores have various chemical and biophysical properties (with solid, liquid or liquid-crystalline phases), and so has the collagenous cap, which influence imaging parameters. MRI has improved its capacity to characterize arterial tissue. This technique can now discriminate the different components of normal and pathological arterial walls through various endogenous or exogenous contrast: intima, media, adventitia, perivascular fat, lipid core, collagenous cap and calcifications of atheromatous plaques, but also precise the elements of plaque resistance to radial stress, or the various factors of inflammation. In the next years, improvement of resolution, new contrast sequences (diffusion or magnetization transfer) or spectroscopy, will compete to allow for the best discrimination of these usual suspects: "the unstable plaques".     

Volumetric Assessment of Plaque Progression With 3-Dimensional Ultrasonography Under Statin Therapy

BACKGROUND AND PURPOSE: Lowering of serum cholesterol levels with HMG-CoA reductase inhibitors (statins) slowed the progression of atherosclerosis in the carotid arteries in several clinical trials using carotid artery intima media thickness as primary outcome measure. Whereas conventional ultrasonography is limited to thin 2-dimensional image planes, 3-dimensional (3D) ultrasonography provides quantitative measurement of the entire carotid artery plaque volume. This study aims to assess the feasibility of 3D ultrasonography to monitor plaque progression in hypercholesterolemic patients. METHODS: The authors prospectively assessed the progression of 31 carotid artery plaques over 15.1 +/- 4.5 months in a study of 23 patients (6 women, 17 men; mean age = 61.7 +/- 7.5 years) with hypercholesterolemia under therapy with HMG-CoA reductase inhibitors. All patients were maintained on a lipid-lowering diet. Sixteen patients were additionally treated with statins. Quantitative measurements of carotid artery plaque volumes were performed after 3D reconstruction of exactly parallel transverse duplex ultrasound scans (slice distance = 0.1 mm) into volumetric 3D data sets and segmentation of voxels representing the carotid artery plaque. RESULTS: Within the treatment group, plaques were significantly less frequently progressive if they had a hypoechoic echogenicity (11%, n = 9 vs 64%, n = 14; P = .016) or if baseline serum cholesterol levels were above 8.0 mmol/L (9%, n = 11 vs 75%, n = 12; P = .002). CONCLUSION: Three-dimensional ultrasonography extends the measurement of the arterial wall thickness to the 3D volume of an entire atherosclerotic plaque including analysis of its morphology and configuration. However, further clinical trials with an adequate sample size to achieve sufficient statistical power are necessary to assess the effect of statin therapy on plaque progression.     

Plasminogen activator inhibitor contributes to the coronary wall thickening in patients with angiographically normal coronary

INTRODUCTION: Angiographically normal coronary arteries have concealed intimal thickening that importantly contribute to coronary arterial disease activity. Increased plasma levels of plasminogen activator inhibitor (PAI) are associated with myocardial infarction and atherosclerosis. However, it remains unclear whether the PAI contributes to vascular wall thickening detected by intravascular ultrasound (IVUS) in normal coronary angiogram. The aim of this study was to evaluate if the PAI activity contributes to the extent of atherosclerotic changes in angiographically normal coronary arteries using IVUS technique. MATERIALS AND METHODS: We studied 33 consecutive patients with normal coronary angiograms. These patients were divided into a high level of plasma PAI activity group (H-PAI; n=12) and a normal range of PAI activity group (N-PAI; n=21), according to the plasma PAI activity levels. RESULTS: The average of "percent intima+media area (%I+M area)" and "maximal intima+media (I+M) thickness" were significantly greater in the H-PAI group as compared with those in the N-PAI group (p<0.05). Minimal lumen diameter and lumen area were comparable between these groups. The plasma PAI activity level was the independent predictor of increase in maximal I+M thickness, in multiple regression analysis with the traditional risk factors as covariates. CONCLUSIONS: Thickened intima+media of angiographically normal coronary arteries were associated with high plasma level of PAI activity, independently of other traditional risk factors. PAI may contribute to the pathogenesis of coronary intimal thickening that might increase coronary arterial tone.     

A modified rabbit model of carotid atherosclerotic plaque suitable for the stroke study and MRI evaluation

In order to induce a modified rabbit model of carotid atherosclerotic plaque suitable for the stroke study and to evaluate the lesion with magnetic resonance imaging (MRI). Eight rabbits of group A were fed with high-fat diet only. Atherosclerosis at the right common carotid artery was induced in rabbits of group B (n = 12) by high-fat diet and balloon catheter injury to the endothelium 4 weeks later. The rabbits were examined in vivo with a 1.5-T MRI. After 4 weeks on the high-fat diet, the serum lipid levels were markedly increased, which became significantly higher than the baseline levels. The lesions on both MRI and histology were remarkable. One week after balloon injury, the signal of injured right common carotid was higher on all the contrast-weighted images than the left side. The extent of abnormal signal was reduced 9 weeks after balloon injury. Hemorrhage was detected on all the contrast-weighted images. In conclusion, the rabbit model established by the authors is such a feasible one to the study of stroke caused by carotid atherosclerosis.     

The independence of maximal intimal thickening from severity of balloon injury in the rabbit aorta

Endothelial injury induces intimal thickening, but whether more extensive injury increases the extent of neointimal proliferation in the rabbit aorta is not well defined. We induced graded injury in the abdominal aortas of rabbits and maximal intimal/medial (I/M) area and thickness ratios were calculated from aortic cross sections harvested 2 weeks after injury. The degree of injury was verified by blinded observers who graded the extent of disruption of the internal elastic laminae. Intimal thickening was not significantly different after severe injury (mean maximal I/M area ratio 0.32+/-0.02 [SE], n = 16) compared with moderate injury (0.23+/-0.02, n = 8, p = 0.24), but was greater than that induced by mild injury (0.08+/-0.01, n = 7, p <0.0001). The ratio of the maximal I/M thickness was similar in all groups (I/M thickness ratio 0.68+/-0.04, 0.73+/-0.04, and 0.56+/-0.04 for severe, moderate, and mild focal injury groups. respectively; p = 0.19). Thus, balloon injury of the rabbit aorta induces reproducible thickening of the intima by 2 weeks. The maximal I/M area ratio is dependent on the extent of injury, while the maximal intimal thickening is independent.     

Correlation between carotid atherosclerosis and serum high-sensitivity C-reactive protein in patients with cerebral infarction

BackgroundSome researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.ObjectiveTo investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis.DesignContrast observation between two groups.SettingDepartment of Neurology, Zhenzhou Hospital, Shenyang Medical College.ParticipantsA total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent.Methods

Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric immunoassay (PENIA) were used for quantitative detection of serum high-sensitivity C-reactive protein.

Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound (Siemens Company, USA) was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria: Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 mm was regarded as normal; 0.9 mm < intima media thickness ≤ 1.2 mm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 mm and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types: steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady.Main outcome measuresThickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups.ResultsAll 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis.

Comparisons of level of high-sensitivity C-reactive protein: Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [(4.66±1.55) mg/L] than the control group [(3.49±1.24) mg/L, t =2.541, P < 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group (P > 0.05).

Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [(8.16±2.42) mg/L] than patients with normal tunica media [(4.66±1.55) mg/L, t =4.132, P < 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [(12.08±3.85) mg/L] than patients with normal tunica media (t =5.994, P < 0.01) and thickening tunica media (t =4.197, P < 0.01).

Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [(13.54±2.62) mg/L] than patients with steady carotid plaque [(8.61±3.71) mg/L, t =2.002, P < 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction.ConclusionSerum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.