Endotoxin inhibits contraction of vascular smooth muscle in vitro.
Endotoxin inhibits contraction of vascular smooth muscle in vitro.
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内毒素在体外抑制血管平滑肌的收缩。
DOI：
10.1152/ajpheart.1990.258.4.h1187
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Levinsky,NG
中科院分区：
文献类型：
--
作者：
Beasley,D;Cohen,RA;Levinsky,NG
血管系统对血管收缩剂的反应性降低与内毒素休克的发病机制有关，但反应性降低的机制尚未确定。在这些研究中，大鼠主动脉环暴露于纯化的大肠杆菌脂多糖（内毒素）在体外抑制随后的收缩引起的血管收缩。内毒素可抑制α-肾上腺素受体激动剂苯肾上腺素引起的收缩，以及钾去极化引起的收缩。内毒素对血管收缩的影响是延迟的。苯肾上腺素诱导的收缩在1小时内暴露于内毒素（10微克/毫升）没有减少，但他们显着减少时，测试数小时后暴露期。1小时暴露于内毒素所引起的抑制的很大一部分是内皮依赖性的。与此相反，内毒素抑制收缩同样在环或不内皮细胞暴露于内毒素较长的时间（3小时）。吲哚美辛不影响内毒素的抑制作用，但在蛋白质合成抑制剂放线菌酮处理的主动脉环中，内毒素的抑制作用被消除。这些研究表明，内毒素在体外有效地抑制血管收缩。内毒素的作用显然不依赖于前列腺素类，但可能涉及蛋白质合成以及对血管平滑肌和内皮细胞的作用。
Decreased responsiveness of the vasculature to vasoconstrictors has been implicated in the pathogenesis of endotoxic shock, yet the mechanism of diminished responsiveness has not been determined. In these studies, exposure of rat aortic rings to purified Escherichia coli lipopolysaccharide (endotoxin) in vitro inhibited subsequent contractions caused by vasoconstrictors. Contractions caused by the alpha-adrenoceptor agonist phenylephrine, as well as those induced by potassium depolarization, were depressed by endotoxin. The effect of endotoxin on vascular contractions was delayed. Phenylephrine-induced contractions were not decreased during a 1-h exposure to endotoxin (10 micrograms/ml), but they were markedly decreased when tested several hours after the exposure period. A large part of the inhibition caused by a 1-h exposure to endotoxin was endothelium dependent. In contrast, endotoxin inhibited contractions equally in rings with or without endothelium exposed to endotoxin for a longer period (3 h). The inhibitory effect of endotoxin was not affected by indomethacin, but it was eliminated in aortic rings treated with the protein synthesis inhibitor cycloheximide. These studies indicate that endotoxin potently inhibits vascular contraction in vitro. The effect of endotoxin is apparently independent of prostanoids but may involve protein synthesis and effects on both vascular smooth muscle and endothelial cells.