Kristof A S, Noorhosseini H, Hussain S N
Critical Care and Respiratory Division, Royal Victoria Hospital, McGill University, Montreal, Québec, Canada.
Eur J Pharmacol. 1997 Jun 5;328(1):69-73. doi: 10.1016/s0014-2999(97)83030-0.
Endothelium-dependent hyperpolarizing factor (EDHF) is an important contributor to agonist-induced vascular dilation. Recent studies suggest that bacterial lipopolysaccharides attenuate endothelium-dependent dilation. Whether or not this effect is mediated through inhibition of EDHF is not known. We studied the in vitro influence of Escherichia coli lipopolysaccharides on endothelium-dependent smooth muscle dilation and hyperpolarization in porcine coronary arteries. Endothelium-intact porcine coronary arterial rings were examined after 20 h of incubation with either saline or E. coli lipopolysaccharides (100 microg/ml). Endothelium-dependent dilation elicited by increasing concentrations of bradykinin was significantly attenuated by lipopolysaccharides. Baseline values of smooth muscle membrane potential were not influenced by lipopolysaccharides. However, lipopolysaccharides significantly attenuated bradykinin-induced smooth muscle membrane hyperpolarization. Our results suggest that attenuation of EDHF is an important mechanism through which lipopolysaccharides influence vascular dilation in severe sepsis.
内皮依赖性超极化因子（EDHF）是激动剂诱导血管舒张的重要促成因素。最近的研究表明，细菌脂多糖会减弱内皮依赖性舒张。这种效应是否通过抑制EDHF介导尚不清楚。我们研究了大肠杆菌脂多糖对猪冠状动脉内皮依赖性平滑肌舒张和超极化的体外影响。用生理盐水或大肠杆菌脂多糖（100微克/毫升）孵育20小时后，检测完整内皮的猪冠状动脉环。脂多糖显著减弱了由浓度递增的缓激肽引起的内皮依赖性舒张。平滑肌膜电位的基线值不受脂多糖影响。然而，脂多糖显著减弱了缓激肽诱导的平滑肌膜超极化。我们的结果表明，EDHF的减弱是脂多糖影响严重脓毒症中血管舒张的重要机制。
