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Hypoxic stress alone does not modulate endothelial surface expression of bovine E-selectin and intercellular adhesion molecule-1 (ICAM-1). 单独的低氧应激不能调节牛e-选择素和细胞间粘附分子-1 (ICAM-1)的内皮表面表达。
Pub Date : 1996-01-01
G Zünd, A L Dzus, D K McGuirk, C Breuer, T Shinoka, J E Mayer, S P Colgan

Unlabelled: Hypoxemia is a common event in many vascular diseases, especially vascular ischemia. Since endothelial cells of blood vessels are exposed to conditions within the vascular space and leucocytes play a key role in ischemia/reperfusion injury, we hypothesized that endothelial exposure to hypoxia may regulate expression of surface proteins important in leucocyte-endothelial interactions, such as E-selectin and intercellular adhesion molecule (ICAM-1). In this study, we used isolated bovine aortic endothelial monolayers to examine endothelial surface alterations of E-selectin and ICAM-1 induced by tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS) and hypoxia using a whole cell enzyme-linked immunosorbent assay (ELISA). Bovine endothelial exposure to TNF-alpha (50 ng/mL) induced a time dependent increase (range 0-24h) in specific E-selection surface expression. Endothelial exposure to hypoxia alone (pO2 approximately 3 mmHg, range 0-24 h), however, failed to elicit endothelial E-selectin expression. Endothelial exposure to LPS brought about a dose- and time-dependent (range 0.5 ng/mL and 2-8 h) increase in specific ICAM-1 surface expression (max. 3.5 +/- 0.15-fold increase over no cytokine control at 10 ng/mL, 4 h). Hypoxia (pO2 approximately 3 mmHg, 8h), however, did not induce ICAM-1 surface expression over normoxia levels.

In conclusion: i) bovine endothelial E-selectin and ICAM-1 surface expression are regulated molecules, ii) hypoxia, per se, does not regulate surface expression of either E-selectin or ICAM-1. These results suggest that hypoxic endothelia may require additional external signals for generation of adaptive inflammatory responses.

低氧血症是许多血管疾病的常见事件,尤其是血管缺血。由于血管内皮细胞暴露于血管空间内,白细胞在缺血/再灌注损伤中起关键作用,我们假设内皮细胞暴露于缺氧可能调节白细胞-内皮相互作用中重要的表面蛋白的表达,如e-选择素和细胞间粘附分子(ICAM-1)。在这项研究中,我们使用分离的牛主动脉内皮单层,用全细胞酶联免疫吸附试验(ELISA)检测了肿瘤坏死因子- α (tnf - α)、脂多糖(LPS)和缺氧诱导的内皮表面e-选择素和ICAM-1的变化。牛内皮暴露于tnf - α (50 ng/mL)诱导特异性e -选择表面表达的时间依赖性增加(范围0-24小时)。然而,内皮细胞单独暴露于缺氧环境(pO2约为3 mmHg,范围0-24 h)不能引起内皮细胞e -选择素的表达。内皮细胞暴露于LPS后,ICAM-1表面特异性表达呈剂量和时间依赖性(范围为0.5 ng/mL, 2-8 h)增加。在10 ng/mL, 4 h时,ICAM-1的表达量比无细胞因子控制时增加了3.5 +/- 0.15倍。然而,缺氧(pO2约为3 mmHg, 8h)在常氧水平下不会诱导ICAM-1表面表达。综上所述:1)牛内皮细胞e -选择素和ICAM-1的表面表达是受调控的分子;2)缺氧本身不调节e -选择素和ICAM-1的表面表达。这些结果表明,缺氧内皮可能需要额外的外部信号来产生适应性炎症反应。
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引用次数: 0
[Self-expanding endoluminal vascular prosthesis: experimental basis and in-vivo evaluation]. 自扩张腔内血管假体:实验基础与体内评价。
Pub Date : 1996-01-01
B Marty, T Marty, L K von Segesser, M Turina

The present study investigates the physical properties and the in vivo application of in vivo of a self-expandable stent (Wallstent) with an incorporated sealant of microporous polyurethane. Measurements of diameter and length as a function axial load featured the data for the calculation for radial pressure. Porosity control was assessed in comparison to non gelatin-sealed knitted Dacron. 11 stents on a 11.5F catheter were inserted in the aorta of three minipigs and evaluated by pressure measurement and angiography. The coverage of the stent causes an increase of 0.05-0.1 bar of radial pressure. The graph received by calculations demonstrates the corresponding pressure for every given diameter of the stents. Porosity is similar to the Dacron graft. The patency-rate is 100%. Characteristics of this covered stents meet requirements of an endovascular prostheses. Exclusion of fistulas and small aneurysms seems to be possible.

本研究研究了微孔聚氨酯密封胶自膨胀支架(Wallstent)的物理性能及其在体内的应用。直径和长度作为轴向载荷的函数的测量为计算径向压力提供了数据。与非明胶密封的针织涤纶相比,评估孔隙度控制。将11个支架置于11.5F的导管上,通过压力测量和血管造影进行评估。支架的覆盖使径向压力增加0.05-0.1 bar。计算得到的曲线图显示了每个给定支架直径对应的压力。孔隙度与涤纶接枝相似。专利率为100%。这种覆盖支架的特性符合血管内假体的要求。排除瘘管和小动脉瘤似乎是可能的。
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引用次数: 0
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Swiss surgery. Supplement
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