Department of Anesthesiology and Intensive Care Medicine, Eberhard-Karls University, Tuebingen, Germany.
Reg Anesth Pain Med. 2010 Jan-Feb;35(1):45-50. doi: 10.1097/AAP.0b013e3181c75199.
The anti-inflammatory effects of local anesthetics (LAs) are well documented. Local anesthetics in micromolar concentrations inhibit extracellular oxygen release in isolated neutrophils; the underlying mechanism seems to be an inhibition of leukocyte priming. It remains unclear, however, if first, these effects also can be observed in whole blood, and second, if the priming of other neutrophil functions is similarly attenuated by LAs. Furthermore, the effects of LAs on intracellular generation of oxidative species remain to be investigated.
Whole-blood samples from healthy volunteers were incubated for 0, 1, or 3 hrs with different concentrations (10 to 10 M) of either lidocaine, ropivacaine, QX314, or NaCl 0.9% as control. Dihydroethidium was added to quantify oxidative burst. Samples were primed with platelet-activating factor (PAF, 10 M) and/or activated with formyl-methyl-leucyl-phenylalanine (10 M) for 15 mins each. After staining for CD11b and lysis of erythrocytes, samples were analyzed by flow cytometry.
Priming of leukocytes is a relevant mechanism in whole blood. Platelet-activating factor stimulates the priming of oxidative burst and CD11b expression. Lidocaine up to millimolar concentrations did not affect the PAF priming and formyl-methyl-leucyl-phenylalanine activation of oxidative burst. The priming of CD11b expression and the priming and activation of changes in cell morphology were significantly attenuated by lidocaine.
The intracellular generation of reactive oxygen species remains largely unaffected by LAs in clinical concentrations. This suggests that the anti-inflammatory effects of LAs do not interfere with the host defense.
局部麻醉剂（LA）具有抗炎作用，这已得到充分证实。在毫摩尔浓度下，局部麻醉剂可抑制分离的嗜中性粒细胞细胞外氧的释放；其潜在机制似乎是抑制白细胞的启动。然而，目前尚不清楚这些作用是否首先可以在全血中观察到，其次，LA 是否同样减弱其他嗜中性粒细胞功能的启动。此外，局部麻醉剂对细胞内氧化物质生成的影响仍有待研究。
健康志愿者的全血样本在不同浓度（10 至 10 M）的利多卡因、罗哌卡因、QX314 或生理盐水 0.9%（作为对照）中孵育 0、1 或 3 小时。加入二氢乙啶以量化氧化爆发。用血小板激活因子（PAF，10 M）和/或甲酰基-甲-亮-苯丙氨酸（10 M）分别对样本进行 15 分钟的启动和激活。用 CD11b 染色并裂解红细胞后，通过流式细胞术对样本进行分析。
白细胞的启动是全血中的一个相关机制。血小板激活因子刺激氧化爆发和 CD11b 表达的启动。利多卡因高达毫摩尔浓度并不影响 PAF 启动和甲酰基-甲-亮-苯丙氨酸激活的氧化爆发。CD11b 表达的启动以及细胞形态变化的启动和激活显著被利多卡因减弱。
在临床浓度下，局部麻醉剂对活性氧的产生几乎没有影响。这表明局部麻醉剂的抗炎作用不会干扰宿主防御。
