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Obesity promotes injury induced femoral artery thrombosis in mice.

机译:肥胖促进小鼠损伤引起的股动脉血栓形成。

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摘要

An FeCl(3) induced femoral arterial thrombosis model was applied to lean (47+/-1.4 g) and obese (64+/-1.7 g) mice (Swiss genetic background) in order to study the relation between obesity and thrombotic risk. As compared to lean mice, obese mice showed a significantly shorter occlusion time (9.9+/-1.0 min versus 13+/-0.5 min; p=0.04) and lower total blood flow (37+/-7.3% versus 69+/-6.7%; p=0.008). A significant negative correlation was observed between body weight and both occlusion time (r=-0.57; p=0.014) and blood flow (r=-0.57; p=0.028). Analysis of the coagulation profile revealed significantly higher levels of plasminogen activator inhibitor-1 (PAI-1), thrombin-antithrombin complex, Factor V activity and combined Factors II/VII/X activity, and moderately elevated Factor VIII activity in obese mice. The degree of arterial damage and the thrombus extension were, however, not significantly different. A significant positive correlation was observed between body weight and either PAI-1 (r=0.63; p=0.003), Factors II/VII/X levels (r=0.80; p<0.0001) or Factor V levels (r=0.65; p=0.003). Thus, this injury induced femoral artery thrombosis model in mice establishes experimentally a correlation between obesity and prothrombotic tendency.
机译:为了研究肥胖与血栓形成风险之间的关系,将FeCl(3)诱导的股动脉血栓形成模型应用于瘦(47 +/- 1.4 g)和肥胖(64 +/- 1.7 g)小鼠(瑞士遗传背景)。与瘦小鼠相比,肥胖小鼠的闭塞时间明显缩短(9.9 +/- 1.0分钟对13 +/- 0.5分钟; p = 0.04),总血流量降低(37 +/- 7.3%对69 +/-) 6.7%; p = 0.008)。体重与闭塞时间(r = -0.57; p = 0.014)和血流量(r = -0.57; p = 0.028)之间均存在显着的负相关。对凝血曲线的分析显示,肥胖小鼠的纤溶酶原激活物抑制剂-1(PAI-1),凝血酶-抗凝血酶复合物,因子V活性和组合的II / VII / X活性明显升高,并且VIII因子活性适度升高。然而,动脉损伤的程度和血栓的延伸没有显着差异。体重与PAI-1(r = 0.63; p = 0.003),因子II / VII / X水平(r = 0.80; p <0.0001)或因子V水平(r = 0.65; p)之间存在显着正相关。 = 0.003)。因此,这种损伤诱发的小鼠股动脉血栓形成模型通过实验建立了肥胖与血栓形成倾向之间的相关性。

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