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SHORT-TERM EXPOSURE TO LIPOPOLYSACCHARIDE IS ASSOCIATED WITH MICROVASCULAR CONTRACTILE DYSFUNCTION IN VIVO

机译:脂多糖的短期暴露与体内微血管收缩功能障碍有关

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The purpose of this study was to determine whether short-term exposure of resistance arterioles to lipopolysaccharide in situ is associated with changes in vasomotor tone. Using intravital microscopy, we found that suffusion of Escherichia coli lipopolysaccharide (3 mu g/ml) over hamster cheek pouch arterioles for 1 h was associated with a significant immediate biphasic response: vasoconstriction followed by vasodilation (p<0.05). The former was attenuated by indomethacin, and the latter by SK&F 108566, a selective, non-peptide angiotensin II receptor antagonist (p<0.05). The nitric oxide synthase inhibitor, N-G-L-nitro arginine, had no significant effects on lipopolysaccharide-induced responses. Allopurinol, a scavenger of reactive oxygen species, significantly attenuated lipopolysaccharide-induced vasodilation. Acetylcholine- and nitroglycerin-induced vasodilation were significantly potentiated after lipopolysaccharide. These responses were recorded in the absence of any significant changes in systemic arterial blood pressure. Collectively, these data suggest that short-term exposure of the peripheral microcirculation to lipopolysaccharide in situ is associated with an ischemia-reperfusion-like injury. These changes may contribute to end organ failure observed several hours after exposure to lipopolysaccharide. [References: 17]
机译:这项研究的目的是确定抗性小动脉在原位脂多糖的短期暴露是否与血管舒缩张力的变化有关。使用活体显微镜检查,我们发现在仓鼠颊袋小动脉上布满大肠埃希氏菌脂多糖(3微克/毫升)持续1 h与显着的双相反应有关:血管收缩,然后血​​管扩张(p <0.05)。前者被消炎痛减毒,后者被选择性的非肽血管紧张素II受体拮抗剂SK&F 108566(p <0.05)。一氧化氮合酶抑制剂N-G-L-硝基精氨酸对脂多糖诱导的反应没有明显影响。别嘌醇是一种活性氧清除剂,可显着减弱脂多糖诱导的血管舒张作用。脂多糖后,乙酰胆碱和硝酸甘油诱导的血管舒张作用明显增强。在系统动脉血压无任何明显变化的情况下记录这些反应。总的来说,这些数据表明外周微循环在原位脂多糖的短期暴露与缺血-再灌注样损伤有关。这些变化可能导致暴露于脂多糖几个小时后观察到的最终器官衰竭。 [参考:17]

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