老年蛛网膜下腔出血后脑血管痉挛患者黏附分子与细胞因子的表达

目的 探讨老年蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)患者黏附分子与细胞因子的表达,以及与脑血管痉挛(CVS)的关系.方法 选择47例老年SAH患者作为病例组并进行功能分级,以及根据是否发生CVS分组;选择同期老年健康体检者40例作为对照组.ELISA法检测血清细胞间黏附分子-1( ICAM-1)和血管细胞黏附分子-1(VCAM-1)以及细胞因子包括白介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达.结果 病例组与对照组比较,黏附分子( ICAM-1、VCAM-1)和细胞因子(IL-6、TNF-α)的表达都明显增高(P＜0.05);且随着功能恶化,其表达也有升高趋势,以上指标在SAH后CVS组的表达显著高于非CVS组(P＜0.05).病例组中,ICAM-1和IL-6、TNF-α以及VCAM-1和IL-6、TNF-α的表达都呈明显的正相关(P＜0.05).结论 老年SAH发生时,患者血清黏附分子和细胞因子的表达显著增高,并且二者表达有密切的关系,共同参与了SAH病情恶化以及CVS的发生.     

细胞间黏附分子-1与脑血管痉挛

细胞问黏附分子-1是黏附分子免疫球蛋白超家族成员之一，在蛛网膜下腔出血后脑血管痉挛形成的病理生理过程中起重要作用，其水平可反映脑血管痉挛程度，并可预测蛛网膜下腔出血的预后。抗细胞问黏附分子-1单抗对脑血管痉挛的治疗有潜在价值。     

脑血管内皮细胞损伤与蛛网膜下腔出血后病理机制的关系

<正>脑血管内皮细胞(brain endothelial cells,BVECs)是脑血管内腔膜表面的单层扁平细胞,是组成血-脑屏障的重要部分,具有调控血液和脑实质之间物质交换的作用。BVECs不仅能感知血液中的炎性因子、微循环中的激素水平、血流压力变化等信息,而且能分泌多种活性物质对这些信息做出调节反应,从而维持正常脑血管功能[1]。BVECs损伤是蛛网膜下腔出血(SAH)后一个重要的病理特征,其与SAH后     

尼莫地平对兔蛛网膜下腔出血后症状性脑血管痉挛的影响

目的探讨尼莫地平对兔蛛网膜下腔出血（SAH）后症状性脑血管痉挛的影响。方法建立症状性脑血管痉挛动物模型，SAH＋尼莫地平组静脉内应用尼莫地平。观察对比神经功能缺损症状改善、血液流变学及电镜结果。结果SAH＋尼莫地平组随着尼莫地平的应用,神经功能缺损症状逐渐好转、血液流变学得到改善、透射电镜见基底动脉病理改变较SAH组减轻。结论SAH后早期应用尼莫地平对症状性脑血管痉挛具有明显的改善作用。     

蛛网膜下腔出血后迟发性脑血管痉挛

迟发性脑血管痉挛是蛛网膜下腔出血的常见并发症,其研究已成为神经病学的热点。文章从脑血管痉挛的发病机制出发,对神经肽Y、一氧化氮、内皮素-1、胆红素氧化产物、Rho激酶、免疫炎症、细胞凋亡等的作用进行了综述。     

蛛网膜下腔出血43例误诊分析

蛛网膜下腔出血(SAH)是临床较常见的疾病,以突发头痛、呕吐、脑膜刺激征为其典型临床表现,并可伴有相应部位神经损害症状、体征,重者可以死亡,因此,及时正确地诊断、治疗相当重要。现总结唐山市人民医院神经内科1995—2005年收治的252例SAH患者中首诊误诊的43例病例的临床资料,以引起临床高度重视。1临床资料43例误诊病例中,男19例,女24例。年龄39~85岁。发病情况:晨起安静状态下发病9例,活动中发病15例,不典型用力后发病13例,发病时间不明确6例。首发症状:发作性眩晕伴呕吐12例;间断性头部跳痛7例;头晕伴血压升高11例;“感冒样”起病11…     

尼莫地平对蛛网膜下腔出血后再出血的影响

目的 探讨蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后应用尼莫地平与再出血的关系,以指导临床合理用药。方法 以307例SAH患者为研究对象,按照确诊SAH给予尼莫地平的时间分为3组,尼莫地平Ⅰ组108例,在发病≤3 d时给予尼莫地平静脉滴注,每日1次,2周后改为口服尼莫地平片30 mg,每日3次;尼莫地平Ⅱ组96例,首次给予尼莫地平距发病时间>3d;对照组103例,确诊为SAH后不用尼莫地平治疗。观察3组再出血情况,进行统计学分析。结果 再出血率以尼莫地平Ⅰ组最低,对照组最高,对Hunt-HessⅡ级的SAH病例,尼莫地平Ⅰ组与对照组比较,x2=4.55,P<05,差异具有显著性意义。其他各组比较差异均无显著性。结论 早期使用尼莫地平预防SAH血管痉挛是安全的,不增加再出血率。     

破裂动脉瘤致蛛网膜下腔出血患者急性期血清单核细胞趋化蛋白1水平的临床意义

目的探讨老年破裂动脉瘤致蛛网膜下腔出血患者急性期血清单核细胞趋化蛋白1(MCP-1)的水平及临床意义。方法脑动脉瘤破裂致蛛网膜下腔出血患者26例(破裂出血组),未破裂动脉瘤患者22例(未破裂组)。另选择同期老年健康体检者25例(对照组),采用ELISA法检测破裂出血组患者出血第1、2、3天血清MCP-1水平,未破裂组患者入院当天血清MCP-1水平及对照组血清MCP-1水平,并进行组间比较。结果破裂出血组患者血清MCP-1水平明显高于未破裂组和对照组,差异有统计学意义(P<0.05)。未破裂组患者血清MCP-1水平与对照组比较,差异无统计学意义(P>0.05)。破裂出血组患者出血后第1、2、3天血清MCP-1水平逐渐升高,但差异无统计学意义(P>0.05)。结论破裂动脉瘤致蛛网膜下腔出血患者急性期血清MCP-1水平升高,且出血急性期逐渐上升,可能参与动脉内外炎性反应。     

抗细胞间黏附分子-1单克隆抗体对老年人中性粒细胞与缺氧内皮细胞黏附的影响

目的测定健康老年人中性粒细胞与人脐静脉内皮细胞细胞株ECV-304的黏附率,探讨抗细胞间黏附分子(ICAM-1,CD54)单克隆抗体对其影响。方法培养的人脐静脉内皮细胞株ECV-304经(或不经)缺氧和抗ICAM-1单抗处理后,分别加入健康老年人中性粒细胞并检测黏附率。结果ECV-304经缺氧处理后,与中性粒细胞黏附率由(21.87±2.47)%增高到(57.05±2.47)%;抗ICAM-1单抗可以部分抑制中性粒细胞与ECV-304黏附,与中性粒细胞黏附率由(21.87±2.47)%降低到(19.55±2.91)%。结论血管内皮细胞在缺氧/复氧后活化,与中性粒细胞之间黏附性增强;ICAM-1参与介导中性粒细胞与血管内皮细胞的黏附,抗ICAM-1单抗可起部分阻断作用。     

蛛网膜下腔出血的治疗

1一般治疗蛛网膜下腔出血(SAH)数小时内的一般治疗:(1)开放气道,改善呼吸、循环;(2)既往血压正常的患者,SAH后血压升高,控制血压使接近正常水平;(3)若有癫痫,抗癫痫治疗包括足量的卡马西平或丙戊酸钠;(4)必要时给予止痛药和镇静剂;(5)对于动脉瘤性SAH,应进行急诊血管造影、血流动力学监测,早期手术。2抗血管痉挛治疗脑血管痉挛是在SAH后,颅底大血管迟发性收缩,常在血管造影或脑血流上表现为受累血管远端区域的灌注减少。造影上血管痉挛有典型的短暂过程-出血后3~5d开始,5~14d狭窄达最大限度,2~4周后逐渐恢复。约半数病例血管痉挛表现为…     

蜂胶水提物预处理对血管内皮细胞的保护作用

目的观察蜂胶水提物对损伤血管内皮细胞的保护作用,探讨蜂胶抗动脉粥样硬化的作用及其机制。方法用50 μg/L TNF-α诱导体外培养脐静脉内皮细胞损伤,用50、100、200 mg/L蜂胶水提物分别干预6、12、24 h,分为对照组、模型组、蜂胶低浓度组、蜂胶中浓度组、蜂胶高浓度组、氟伐他汀钠组、联合组,采用流式细胞仪检测细胞间黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)的表达。结果与对照组比较,模型组ICAM-1和VCAM-1表达明显升高;与模型组比较,蜂胶低浓度组、蜂胶中浓度组和蜂胶高浓度组ICAM-1和VCAM-1明显降低(P0.01)。12 h时与氟伐他汀钠组比较,联合组ICAM-1和VCAM-1表达明显降低(P0.01)。结论蜂胶水提物能降低ICAM-1和VCAM-1的表达。与氟伐他汀钠联合应用,对血管内皮细胞损伤有协同保护作用。     

辛伐他汀对兔实验性动脉硬化引起的内皮功能失调的保护作用

目的 评估辛伐他汀对于胆固醇喂养兔的血管内皮影响。方法 １４只新西兰大白兔喂以高胆固醇饲料（１％胆固醇）１０周，在４周后随机分为两组，一组（Ｂ组）继续给高胆固醇饲料，一组（Ｃ组）为高胆固醇饲料加辛伐他汀（２ｍｇ．ｋｇ＾－１．ｄ＾－１）。第三组（７只，Ａ组），给予标准饲料，１０周后取血测血脂包括总胆固醇，低，高密度脂蛋白－胆固醇及甘油三酯。麻醉后分离胸主动脉去除结缔组织及脂肪组织，取近主动脉弓处一小     

Effects of density and of dehydration of sickle cells on their adhesion to cultured endothelial cells

Abnormal adhesion of sickle cells to vascular endothelium may be a factor in the initiation of painful vaso-occlusive crisis. The sickle cell population contains an unusually large number of less dense reticulocytes that are known to be more adhesive than mature red cells, but there is contradictory evidence regarding the adhesiveness of dense sickle cells. We used a flow-based assay of adhesion to cultured human umbilical vein endothelial cells to test the properties of density fractions of sickle cells, prepared either by density gradient or by centrifugation of packed cells. We also examined the effects of incubating sickle cells with or without cyclical deoxygenation on their adhesion. After fractionation on a Percoll-Isopaque gradient, the less dense 10% (reticulocyte-rich) cells and the most dense 10% cells adhered in greater number than the remainder (by about twofold). However, after centrifugation of packed cells, the less dense 10% were again more adhesive than the “middle” cells, but the most dense were not. Exposing sickle cells to constituents of the gradient had no consistent effect on adhesion, while centrifugal packing induced a degree of hemolysis, and tended to reduce adhesiveness of the dense fraction previously obtained from a gradient. Incubation in air at 37°C for 15 hr reduced the number of reticulocytes and the adhesiveness of less dense sickle cells compared to those held at 4°C. On the other hand, incubation at 37°C for 15 hr with cyclical deoxygenation caused formation of dense cells and increased adhesiveness compared to incubation without cyclical deoxygenation. We conclude that young, less dense sickle cells are unusually adhesive, but that this adhesiveness is reduced during maturation. However, repeated sickling in vivo causes formation of an abnormally dense subpopulation of cells which either redevelop an increased tendency to adhere to endothelial cells or preserve their initial adhesiveness. Both adhesive cell populations may be implicated in promoting vascular obstruction. © 1996 Wiley-Liss, Inc.     

Ghrelin对同型半胱氨酸诱导大鼠心肌微血管内皮细胞损伤和炎性反应的保护作用

目的探讨Ghrelin对同型半胱氨酸(Hcy)诱导大鼠心肌微血管内皮细胞(CMECs)损伤和炎性反应的保护作用及作用机制。方法取雄性SD大鼠心肌细胞培养鉴定后,分别以不同浓度的Hcy、不同浓度Ghrelin孵育24 h,采用MTT法检测细胞活力。另选细胞随机分为对照组、Hcy组(0.25 mmol/L)、Ghrelin组(100 ng/L)和混合组,Hoechst染色计算细胞凋亡率,NO试剂盒检测NO的分泌活性,ELISA检测白细胞介素6(IL-6)、细胞间黏附分子1(ICAM-1)的分泌,免疫印迹法检测NF-κB蛋白的表达。结果不同浓度Hcy细胞活性较不同浓度Ghrelin明显降低(P0.05,P0.01)。与对照组比较,Hcy组NO的分泌活性显著降低,细胞凋亡率显著上升,IL-6和ICAM-1的分泌显著增加,NF-κB的表达显著增加,差异有统计学意义(P0.05,P0.01)。与Hcy组比较,混合组可以明显抑制上述指标(P0.05)。结论 Hcy可诱发大鼠CMECs的损伤和炎性反应,而Ghrelin预处理对Hcy诱导的损伤及炎性反应有明显的抑制作用,其保护作用机制可能与抑制NF-κB信号通路有关。     

蜕皮甾酮对胰岛素抵抗HepG2细胞胰岛素受体表达的影响

目的 探讨蜕皮甾酮对胰岛素抵抗(IR)HepG2细胞胰岛素受体(InsR)蛋白表达的影响.方法 建立胰岛素抵抗HepG2细胞模型,培养液中加入蜕皮甾酮孵育,观察蜕皮甾酮及吡格列酮对细胞葡萄糖摄取率的影响;应用免疫组化染色法及Western blot方法观察蜕皮甾酮对IR HepG2细胞InsR蛋白表达的影响. 结果 与模型细胞比较,1×10-5 mol/L蜕皮甾酮可使IR HepG2细胞InsR蛋白的表达显著增加. 结论 蜕皮甾酮的胰岛素增敏作用可能与胰岛素信号转导分子InsR蛋白的表达增强有关.     

Enhanced endothelial activation in diabetic patients with unstable angina and non-Q-wave myocardial infarction.

AIMS: Diabetes mellitus (DM) is associated with chronic endothelial dysfunction. Diabetic patients presenting with acute coronary syndromes have a worse prognosis than non-diabetics. An acute inflammatory reaction at the site of coronary plaque rupture and increased expression of surface and soluble cellular adhesion molecules (CAMs) are pathological features of acute coronary syndromes. We set out to characterize the expression of soluble CAMs in patients with and without diabetes presenting with unstable angina (UA) and non Q-wave myocardial infarction (NQMI). METHODS: Patients presenting with UA and NQMI had serum samples taken on presentation, after 72 h and then 3, 6 and 12 months after discharge. Levels of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin and P-selectin were measured using an ELISA technique. RESULTS: We studied 15 diabetic patients and 15 age- and sex-matched non-diabetic patients presenting with either UA or NQMI. Levels of soluble E-selectin were elevated in the diabetic patients in comparison with the non-diabetic patients at all measured time points: 74 +/- 10 ng/ml vs. 47 +/- 3 ng/ml, P < 0.03 at t = 0 h, 55 +/- 5 ng/ml vs. 38 +/- 2 ng/ml, P < 0.02 at t = 72 h. However, levels of soluble P-selectin were lower in the diabetic cohort during follow-up: 134 +/- 15 ng/ml vs. 225 +/- 32 ng/ml, P < 0.02 at t = 3/12 and 112 +/- 8 ng/ml vs. 197 +/- 23 ng/ml, P < 0.02 at t = 6/12. There was no significant difference in levels of soluble ICAM-1 and VCAM-1 between diabetic and non-diabetic patients. CONCLUSIONS: Levels of soluble E-selectin are significantly elevated in diabetic patients presenting with UA and NQMI in comparison with non-diabetics. This finding may reflect enhanced endothelial activation which may contribute to the adverse prognosis of diabetic patients with acute coronary syndromes.     

High expression of the focal adhesion- and microfilament-associated protein VASP in vascular smooth muscle and endothelial cells of the intact human vessel wall

The focal adhesion and microfilament-associated protein VASP is a major substrate of both cAMP- and cGMP-dependent protein kinase in intact human platelets. The recent elucidation of the primary VASP structure and identity of VASP binding proteins suggest that VASP is an important component of focal contacts which link signal transduction pathways and elements controlling cell motility. In this study, the high expression of VASP in vascular smooth muscle and endothelial cells of human blood vessels is reported. Western blot and immunofluorescence analysis detected VASP in human heart, femoral artery and a uterine leiomyosarcoma. Within these tissues, smooth muscle cells, small capillaries and the endothelial cell layer were strongly stained by the VASP antiserum. In human heart, an overlapping cellular distribution of the cGMP-dependent protein kinase I (cGK I) and its substrate VASP was noted. Immunoelectron microscopy experiments with vascular smooth muscle cells of the vessel wall revealed that VASP is localized in close proximity to microfilaments, dense plaques and dense bodies. The data of this study and the properties of VASP as a major target of inhibitory vasoactive agents suggest that VASP is an important component which participates in the regulation of cell motility of human vessel wall cells in vivo.Abbreviations VASP Vasodilator stimulated phosphoprotein - cGK I cGMP-dependent protein kinase type I - cAK cAMP-dependent protein kinase - EC endothelial cell - SMC smooth muscle cell