Atherosclerosis following balloon catheter injury to the carotid artery and the aorta of hypertensive rats with normolipidemia or hyperlipidemia.

The carotid artery and abdominal aorta of hypertensive normocholesterolemic rats responded in similar manner to balloon denuding of the endothelium. One denuding resulted in an intimal fibrous plaque, while multiple such injuries increased the lipid content of the plaque and so yielded fatty-fibrous plaques, which perhaps represent an intermediate stage of atherosclerosis. In no instance did a single or multiple denuding lead to advanced atherosclerosis. Although the abdominal aorta of animals with one or with repeated denudings accumulated more lipid when placed on atherogenic died, the lesions remained essentially in the fatty-fibrous plaque category. Typical atherosclerosis was observed only occasionally and was limited to rats with multiple denudings. In rats with denuded carotid artery on an atherogenic diet classic atherosclerosis developed, especially when there were multiple episodes of injury. This was the first time the authors observed advanced atherosclerosis in the rat, and the lesions were quite comparable to human atherosclerosis. For the rat in this instance the principal factors in pathogenesis were hyperlipidemia and the repeated endothelial denudings, which promoted lipid deposit in the intimal plaques of the vessel.     

Hemifacial spasm patient with ipsilateral total absence of common carotid artery, vertebral artery and aneurysm of the contralateral internal carotid artery

We present a case of a 45-year-old male patient with left hemifacial spasm for 6 years. Magnetic resonance tomographic angiography confirmed that there were small vessels adjacent to the left facial nerve root entry zone, but the left internal carotid artery (ICA) was absent. Magnetic resonance angiography using three-dimensional time of flight technique showed the absence of the left ICA and vertebral artery, But the presence of a 6-mm aneurysm in the bifurcation of the right internal carotid artery. These abnormal arterial structures were further confirmed by angiogram. Aortic arch angiogram revealed a right-sided aortic arch and the Subclavian steal phenomenon. The left common carotid artery and the left Subclavian artery were absent. Right vertebral angiography showed retrograde filling of the left vertebral artery. The left upper limb was fed by this artery. The aneurysm was successfully clipped. Post-operatively, the hemifacial spasm was weakened. However, the operation did not change the neurovascular positional relationship, thus we advised follow-up visits. Cerebral artery anomalies should be taken into consideration when performing imaging and surgical corrections in patients with hemifacial spasm.     

Responses of inner and outer muscle of the sheep carotid artery to injury.

1. Direct injury to the smooth muscle of the sheep carotid artery in vivo caused large, persistent and sharply limited annular contraction, even with tetrodotoxin 10(-5)M present to block nerves. 2. Surcose gap records from artery strips showed that mechanical injury caused slow, prolonged depolarization of the smooth muscle that spread for a few millimetres in a circular direction in relation to the intact artery wall with an apparent space constant of 1-26--3.49 mm. In the longitudinal direction, no depolarization was recorded 1 mm from the site of injury. No spikes were recorded more than 1 mm in either direction from the site of injury except when procaine, which facilitates electrical activity in the smooth muscle, was present. 3. When responses of inner and outer muscle were recorded separately, injury caused comparable contraction of both parts. 4. Clotted blood caused large contractions of intact artery strips; it contracted inner much more than outer muscle. 5. The main factors in the intact vessel's response to injury therefore seem to be inner and outer muscles' direct response to injury, reinforced by spread of depolarization round the vessel wall, and inner muscle's response to vasoconstrictor agents released by clotting blood.     

Flow analysis in vascular shunts that bypass the carotid artery.

When blood flow through a carotid artery is impaired and vascular surgery is necessary to restore adequate circulation a vascular shunt can be applied to maintain cerebral blood flow. Several vascular shunts are commercially available, but there is only limited test data on their flow capacity. The purpose of this study is to determine the flow capacity of three vascular shunt systems. A theoretical model has been developed for this purpose. To validate the model, in vitro flow measurements were taken. Application of the model showed that all shunts cause a decrease in blood flow. The amount of flow decrease varied widely from 13% (Javid shunt) to 55% (Pruitt-Inahara). In vitro measurements confirmed the validity of the model. In conclusion, it is important for the vascular surgeon to realise that vascular shunts show large differences in flow capacity. Of the three investigated shunts, the Javid has the highest flow capacity.     

B(2)-receptor modulation of the reactivity to phenylephrine and angiotensin II in the carotid artery of normotensive rats after trandolapril treatment.

This study was designed to study the effects of angiotensin converting enzyme inhibitors (ACEI) following treatment with trandolapril (0.3 mg kg(-1) day(-1)) on carotid arterial responsiveness in normotensive Wistar rats. Carotid arteries were obtained from control or trandolapril-treated animals and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and KCl was studied. Agonist concentration-response curves were constructed in either the absence or presence of the endothelium or after incubation with L-NAME (10(-6) M), HOE140 (10(-7) M) or indomethacin (10(-5) M). Trandolapril treatment decreased the Ang II and Phe potencies in carotid arteries, but did not affect the maximal response. The KCl responses (potency and Emax) were similar in both control and trandolapril-treated arteries. The absence of endothelium increased the response to both agonists in control and trandolapril-treated arteries; however, the inhibitory component from the endothelial layer of the Phe response was greater in trandolapril-treated animals than in control animals. The presence of L-NAME or HOE140 abolished the changes in the potency values of trandolapril-treated animals. The presence of indomethacin did not change the effect of trandolapril on the potency values of both agonists. We conclude that trandolapril treatment decreased the carotid arterial reactivity in normotensive rats and that this effect is endothelium-dependent. Furthermore, the involvement of B(2)-receptors and NO production, but not of prostaglandins, is suggested in this mechanism.     

Influence of heat stress on the reactivity of isolated chicken carotid artery to vasoactive agents

Cerebral ischaemia is considered to be an important cause of central nervous system dysfunction in heat stress. We hypothesized that heat stress would alter the reactivity of isolated carotid artery to vasoactive agents. Carotid arteries were isolated from broiler chickens maintained either at 23-24 degrees C with 55-65% humidity (control conditions) or exposed to 40 +/- 1 degrees C with 35% humidity for 4 h (heat stress). Contractions were elicited with vasoconstrictors such as 5-HT, phenylephrine, guanfacine and CaCl(2) (K(+)-depolarized) in endothelium-denuded arterial rings. Heat stress significantly increased the potency of 5-HT, but had no effect on the sensitivity of the vessel to phenylephrine or guanfacine. In contrast, it markedly decreased the potency and efficacy of CaCl(2). Vasodilator responses to ACh (endothelium-intact) and sodium nitroprusside (endothelium-denuded), however, were unaffected. Although cyclopiazonic acid (10 microm) significantly decreased 5-HT responses in both the conditions, the agonist was still more potent in heat stress. Extracellular Ca(2)(+) removal had no effect on contractions caused by 5-HT in control conditions, but it significantly decreased the agonist potency in heat stress. Interestingly, nifedipine (1 microm) markedly inhibited 5-HT-induced contractions both in control conditions and in heat stress, implying an inhibitory effect on both Ca(2)(+) influx and release. Thus, nifedipine had a markedly greater inhibitory effect on 5-HT-induced contractions in heat stress compared with control conditions. The results suggest that heat stress increased the vasoconstrictor responses to 5-HT by a mechanism that involved extracellular Ca(2)(+) influx through nifedipine-sensitive L-type calcium channels.     

Endothelialization and patency of RGD-functionalized vascular grafts in a rabbit carotid artery model

To address the growing demand of small-diameter vascular grafts for cardiovascular disease, it is necessary to develop substitutes with bio-functionalities, such as anticoagulation, rapid endothelialization, and smooth muscle regeneration. In this study, the small-diameter tubular grafts (2.2 mm) were fabricated by electrospinning of biodegradable polymer polycaprolactone (PCL) followed by functional surface coating with an arginine-glycine-aspartic acid (RGD)-containing molecule. The healing characteristics of the grafts were evaluated by implanting them in rabbit carotid arteries for 2 and 4 weeks. Results showed that at both time points, all 10 of the RGD-modified PCL grafts (PCL-RGD) were patent, whereas 4 of the 10 non-modified PCL grafts were occluded due to thrombus formation. Scanning electron microscopy (SEM) data showed abundant platelets adhering on the surface of the midportion of the PCL grafts. In contrast, only few platelets were observed on the PCL-RGD surface, suggesting that RGD modification significantly improved the hemocompatibility of the PCL grafts. Histological analysis demonstrated enhanced cell infiltration and homogeneous distribution within the PCL-RGD grafts in comparison with the PCL grafts. Furthermore, immunofluorescence staining also showed a 3-fold increase of endothelial coverage of the PCL-RGD grafts than that of PCL grafts at those two time points. After 4-week implantation, 65.3 ± 7.6% of the surface area of the PCL-RGD grafts was covered by smooth muscle cell layer, which is almost 23% more than that on the PCL grafts. The present study indicates that RGD-modified PCL grafts exhibit an improved remodeling and integration capability in revascularization.     

构建颈动脉损伤模型大鼠早期生长反应因子1及组织因子的表达

背景：脱氧核酶ED5可通过特异性抑制早期生长反应因子1的表达来阻遏下游靶基因的表达。 目的：构建颈动脉损伤模型大鼠,观察早期生长反应因子1的脱氧核酶ED5对大鼠颈动脉损伤后血浆组织因子水平的影响及防治血管内膜增生的机制。 方法：实验采用左颈总动脉内膜剥脱构建颈动脉球囊损伤模型大鼠,分别将ED5,MgCl2和FuGene6注入大鼠损伤的血管节段内。 结果与结论：病理学检查、免疫荧光染色、免疫组织化学染色、ELISA检测结果显示,建模后3,7,14,21 d,与MgCl2组和FuGene6组相比,经损伤动脉局部转染ED5后的大鼠血管组织早期生长反应因子1的表达和血浆组织因子的表达水平明显减少(P < 0.01),且建模后7,14,21 d内膜增生程度明显减轻(P < 0.01)。结果证实,早期生长反应因子1特异脱氧核酶ED5可能通过抑制组织因子的表达,从而抑制损伤颈动脉内膜的增生。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

卡维地洛对大鼠颈动脉损伤后血管重塑的影响

目的:探讨卡维地洛(carvedilol,CAR)对大鼠颈动脉损伤后血管重塑的影响.方法:雄性Wistar大鼠90只,随机分为假手术组、损伤组和CAR组,后两组行颈动脉球囊损伤术.三组均于术后1、3、7、14、28天处死大鼠.光镜下观察血管损伤后内膜增生情况,用免疫组化和RT-PCR法检测MMP-2、MMP-9和TIMP-1在各组术后不同时间点的表达情况.结果:与损伤组比较,术后14dCAR组内膜面积、内膜与中膜面积比值显著减少,管腔面积显著扩大(P<0.05);与损伤组比较,CAR组术后3-14dMMP-2、MMP-9表达显著减少(P<0.05),而TIMP-1表达无显著变化(P>0.05).结论:卡维地洛有效抑制大鼠颈动脉损伤后MMP-2和MMP-9表达,改善了细胞外基质的合成与降解平衡,抑制血管重塑,减轻再狭窄.     

Effect of hypoxia on vascular responses to the carotid baroreflex.

The effect of systemic hypoxia on the vascular responses to the carotid baroreflex was studied in anesthetized, vagotomized, artificially ventilated dogs. One hindlimb, kidney, gracilis muscle, and paw were perfused at constant flow, and neurograms were obtained from renal sympathetic fibers. Bilateral carotid occlusions were performed while the animal was breathing a mixture of air and O2 (mean arterial PO2 = 106 mmHg) and again during ventilation with 10% O2 (PO2 = 40 mmHg). With occlusion, the average increase in mean aortic pressure was 36 mmHg greater during hypoxia than during normoxia and the increase in renal perfusion pressure was 87 mmHg greater; the increase in hindlimb perfusion pressure was identical in both situations. Hypoxia did not change the reflex response of the paw to carotid occlusion and increased that of the muscle vessels by only 10%; the increase in renal sympathetic activity averaged 56 plus or minus 10% more with hypoxia than with normoxia. When the carotid chemoreceptors were destroyed, the greater increase in aortic and renal pressure response to carotid occlusion during hypoxia as compared to normoxia was abolished. Thus systemic hypoxia markedly potentiates the reflex renal constriction caused by the baroreflex, and this effect is due to the carotid chemoreceptor afferent input.     

Physical training under the influence of beta-blockade in rats. II: Effects on vascular reactivity

Summary Rats were treated by daily swimming or running exercises for 7 weeks. One group of rats was also trained under the influence of propranolol, while another group received daily propranolol injections only.The rat groups trained without beta blockade maintained a higher tail skin temperature when exposed to 5 C after the 7-week training period. This phenomenon was not observable in the animals having received their training under the influence of beta-blockade. Both rat groups trained without beta-blockade showed increased vasodilatatory response to isoprenaline, as judged from a higher elevation of the tail skin temperature in response to the drug. This response was absent in the animal group having performed its training periods under the influence of propranolol. After the injection of phenylephrine the trained rats had a higher tail skin temperature than did the controls or propranolol-treated rats.The present results suggest an elevated sensitivity of beta₂-adrenoceptors and/or decreased sensitivity of alpha-adrenoceptors in trained rats. It is suggested that for the development of these changes repeated activation of the sympathetic nervous system by exercise periods is needed. That is why they are preventable if the training is performed under the influence of beta-blockade.     

RhoA调节失血性休克大鼠血管反应性的机制

目的： 探讨RhoA调节失血性休克大鼠血管反应性的机制。方法: 采用SD大鼠复制休克模型,取离体血管环,观察Rho激酶、肌球蛋白轻链磷酸酶（MLCP）、肌球蛋白轻链磷酸激酶（MLCK）对RhoA增加血管反应性的作用;同时取原代血管平滑肌细胞（VSMCs）,观察RhoA对缺氧后VSMC Rho激酶、MLCP和MLCK活性的调节作用以及对肌球蛋白轻链（MLC20）磷酸化水平的影响。结果: 失血性休克后大鼠肠系膜上动脉（SMA）对NE收缩反应性明显降低,RhoA的激动剂U-46619可明显升高休克后血管反应性,RhoA特异性抑制剂C3酶可拮抗U-46619所引起的血管收缩反应性的升高。Rho激酶抑制剂Y-27632可降低由U-46619所引起的血管反应性的升高,MLCP的抑制剂Calyculin可进一步增加由U-46619所引起的血管反应性的升高,而MLCK抑制剂对U-46619的作用影响不明显。缺氧后MLCK、Rho激酶活性以及MLC20磷酸化水平明显降低,MLCP活性明显升高,RhoA激动剂U-46619可明显升高缺氧后VSMC的MLC20磷酸化水平、Rho激酶活性和降低MLCP的活性,且U-46619的这一作用可被RhoA抑制剂C3酶所拮抗,调节RhoA的活性对MLCK活性无明显调节作用。结论: RhoA可通过Rho激酶调节MLCP活性和 MLC20磷酸化水平调节休克后血管反应性。     

颈动脉分叉区域的神经血管解剖及其对颈动脉内膜剥脱术的临床意义

目的　通过对尸体标本的颈动脉分叉区域内的神经、血管进行解剖研究,为安全有效地开展颈动脉内膜剥脱术提供形态学依据及解剖学基础。 方法 选取20例（40侧）无明确心、脑血管疾患的尸体解剖标本（男11例、女9例）,采取颈动脉内膜剥脱术式入路对颈动脉分叉区域内的神经、血管进行解剖研究,明确血管和神经的形态学及结构特点。 结果 颈总动脉分叉部形态可分为Ⅰ、Ⅱ、Ⅲ型,分别占比为10%、52.5%、37.5%。分叉位置以甲状软骨为界,左侧颈总动脉分叉部高度在其上缘以上、平上缘和上缘以下的占比分别为55%、37.5%、7.5%;相较之下右侧分别为62.5%、27.5%、10%。男性颈总、颈内、颈外动脉内径均大于女性（P<0.05）;男性颈动脉分叉角度大于女性（P<0.05 ）。双侧颈总、颈内、颈外动脉内径相比无统计学意义（P>0.0 5）;左侧颈动脉分叉角度大于右侧（P<0.05）。 结论　通过对颈动脉分叉区域内的神经、血管进行解剖研究,对颈动脉内膜剥脱术术中血管与神经的保护具有重要的临床意义。     

Prevention of vascular injury to the spinal cord incidence of a great posterior radicular artery

This study investigated in 165 cadavers for the presence and morphology of a great posterior radicular artery (GPRA). The spinal cords were examined for the presence of a GPRA macroscopically and by stereomicroscopy, and the spinal segmental level where the GPRA was located and left-right differences were investigated. A GPRA was found to be present in 10 (6.1%) of the 165 cadavers, and a solitary unilateral GPRA was observed on the left or right side of the spinal cord in each of them. While no differences in laterality were identified, the GPRA was most often seen at the level of the spinal segment T11. The mean outer diameter of the GPRA was 0.43 mm. No previous studies have described the GPRA in a Japanese population. In the 10 cadavers in which a GPRA found in this study its most common location was at the level of spinal segment Th11. There was a difference of more than 2 spinal segmental levels between the location of the artery in our study and in a European population, suggesting that the spinal segmental level at which the GPRA is located is 1 or 2 levels higher in the Japanese population.     

跨膜蛋白66过表达减轻大鼠颈动脉球囊损伤后内膜增生

目的研究跨膜蛋白66(TMEM66)在大鼠颈动脉球囊损伤后内膜增生中的作用。方法将SD大鼠随机分为对照组,左侧颈动脉球囊损伤组和TMEM66过表达组(n=10)。HE染色检测各组血管内膜增生情况。Western blot、q-PCR及IHC分别检测颈动脉血管中TMEM66的表达。CCK8和划痕实验分别检测TMEM66过表达后原代培养血管平滑肌细胞(VSMC)的增殖和迁移。结果颈动脉球囊损伤血管中TMEM66的表达量较对照组显著下降(P0.05)。球囊损伤后血管内膜明显增生,慢病毒特异性转染TMEM66过表达可显著逆转血管内膜增生(P0.05)。上调TMEM66能够改善PDGF所诱导的VSMC增殖和迁移(P0.05)。结论 TMEM66可以改善大鼠颈动脉球囊损伤后内膜增生。     

同型半胱氨酸对大鼠血管内皮依赖性舒张反应的影响

目的：观察同型半胱氨酸对内皮依赖性舒张反应的影响。方法：Wistar大鼠24只,随机分为两组。实验组腹腔内注射同型半胱氨酸溶液100 mg·kg^-1·d^-1;对照组注射等量生理盐水。第16周末,测血清同型半胱氨酸浓度、扫描电镜检查颈总动脉内皮细胞并测定离体内皮依赖性舒张功能。结果：实验组血清同型半胱氨酸显著高于对照组。扫描电镜观察,实验组内皮细胞表面收缩、凹凸不平、细胞间隙增宽,部分区域可见片状脱落;实验组的血管环对乙酰胆碱浓度依赖性舒张反应明显下降。结论：同型半胱氨酸对血管内皮细胞有损伤作用,进而降低内皮依赖性舒张功能。     

Quality evaluation of ultrasound imaging in the carotid artery based on normalization and speckle reduction filtering

Image quality is important when evaluating ultrasound images of the carotid for the assessment of the degree of atherosclerotic disease, or when transferring images through a telemedicine channel, and/or in other image processing tasks. The objective of this study was to investigate the usefulness of image quality evaluation based on image quality metrics and visual perception, in ultrasound imaging of the carotid artery after normalization and speckle reduction filtering. Image quality was evaluated based on statistical and texture features, image quality evaluation metrics, and visual perception evaluation made by two experts. These were computed on 80 longitudinal ultrasound images of the carotid bifurcation recorded from two different ultrasound scanners, the HDI ATL-3000 and the HDI ATL-5000 scanner, before (NF) and after (DS) speckle reduction filtering, after normalization (N), and after normalization and speckle reduction filtering (NDS). The results of this study showed that: (1) the normalized speckle reduction, NDS, images were rated visually better on both scanners; (2) the NDS images showed better statistical and texture analysis results on both scanners; (3) better image quality evaluation results were obtained between the original (NF) and normalized (N) images, i.e. NF–N, for both scanners, followed by the NF–DS images for the ATL HDI-5000 scanner and the NF–DS on the HDI ATL-3000 scanner; (4) the ATL HDI-5000 scanner images have considerable higher entropy than the ATL HDI-3000 scanner and thus more information content. However, based on the visual evaluation by the two experts, both scanners were rated similarly. The above findings are also in agreement with the visual perception evaluation, carried out by the two vascular experts. The results of this study showed that ultrasound image normalization and speckle reduction filtering are important preprocessing steps favoring image quality, and should be further investigated.     

缺血预处理对失血性休克大鼠血管反应性及钙敏感性的影响

目的：观察缺血预处理对失血性休克血管反应性和钙敏感性的影响。方法：通过观察不同缺血预处理方法对失血性休克大鼠存活时间和24 h存活率的影响,选择最适缺血预处理方法。在体实验,观察缺血预处理对失血性休克大鼠肠系膜上动脉（SMA）血管管径对去甲肾上腺素（NE）收缩反应性和NE升压反应的影响;离体实验,应用离体血管环张力测定技术,观察缺血预处理对失血性休克后大鼠SMA环血管反应性和钙敏感性的影响。结果：确定最适缺血预处理方法为：夹闭腹主动脉1 min,开放5 min,重复3次,2 h后复制失血性休克模型,这种方法可显著增加失血性休克大鼠的存活时间和24 h存活率。在体实验,缺血预处理可显著增加休克晚期NE的升压效应和在体SMA对NE的收缩反应（P<0.01）。离体实验,与失血性休克对照组比较,缺血预处理组SMA在休克早期(休克即刻)对NE的收缩反应性和钙敏感性明显下降（P<0.05）,但与正常对照组比较无显著差异（P>0.05）;在休克后期（休克2 h、3 h、4 h）,缺血预处理组SMA对NE的收缩反应性和钙敏感性显著增加（P<0.05）,且与正常对照组比较无显著差异（P>0.05）。结论：缺血预处理可能通过改善血管钙敏感性发挥对休克后期血管反应性的保护效应。