Department of Anesthesiology, Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Centre, Meibergdreef Amsterdam, The Netherlands.
Anesthesiology. 2013 Jan;118(1):95-104. doi: 10.1097/ALN.0b013e3182751300.
Helium protects myocardium by inducing preconditioning in animals. We investigated whether human endothelium is preconditioned by helium inhalation in vivo.
Forearm ischemia-reperfusion (I/R) in healthy volunteers (each group n = 10) was performed by inflating a blood pressure cuff for 20 min. Endothelium-dependent and endothelium-independent responses were measured after cumulative dose-response infusion of acetylcholine and sodium nitroprusside, respectively, at baseline and after 15 min of reperfusion using strain-gauge, venous occlusion plethysmography. Helium preconditioning was applied by inhalation of helium (79% helium, 21% oxygen) either 15 min (helium early preconditioning [He-EPC]) or 24 h before I/R (helium late preconditioning). Additional measurements of He-EPC were done after blockade of endothelial nitric oxide synthase. Plasma levels of cytokines, adhesion molecules, and cell-derived microparticles were determined. Forearm I/R attenuated endothelium-dependent vasodilation (acetylcholine) with unaltered endothelium-independent response (sodium nitroprusside). Both He-EPC and helium late preconditioning attenuated I/R-induced endothelial dysfunction (max increase in forearm blood flow in response to acetylcholine after I/R was 180 ± 24% [mean ± SEM] without preconditioning, 573 ± 140% after He-EPC, and 290 ± 32% after helium late preconditioning). Protection of helium was comparable to ischemic preconditioning (max forearm blood flow 436 ± 38%) and was not abolished after endothelial nitric oxide synthase blockade. He-EPC did not affect plasma levels of cytokines, adhesion molecules, or microparticles.
Helium is a nonanesthetic, nontoxic gas without hemodynamic side effects, which induces early and late preconditioning of human endothelium in vivo. Further studies have to investigate whether helium may be an instrument to induce endothelial preconditioning in patients with cardiovascular risk factors.
氦气通过在动物体内诱导预处理来保护心肌。我们研究了人类内皮细胞是否通过吸入氦气在体内被预处理。
通过充气血压袖带 20 分钟,在健康志愿者(每组 n = 10)的前臂缺血再灌注(I/R)中进行。在基线和再灌注 15 分钟后,使用应变计、静脉闭塞体积描记法,分别在累积剂量反应输注乙酰胆碱和硝普钠后,测量内皮依赖性和非内皮依赖性反应。通过吸入氦气(79%氦气,21%氧气)在 I/R 前 15 分钟(氦气早期预处理[He-EPC])或 24 小时(氦气晚期预处理)进行氦气预处理。在阻断内皮一氧化氮合酶后,对 He-EPC 进行了额外的测量。测定细胞因子、粘附分子和细胞衍生的微颗粒的血浆水平。前臂 I/R 减弱了内皮依赖性血管舒张(乙酰胆碱),而内皮非依赖性反应(硝普钠)不变。He-EPC 和氦气晚期预处理均减弱了 I/R 诱导的内皮功能障碍(I/R 后乙酰胆碱反应引起的前臂血流最大增加在无预处理时为 180 ± 24%[平均值 ± SEM],He-EPC 后为 573 ± 140%,氦气晚期预处理后为 290 ± 32%)。氦气的保护作用与缺血预处理相当(最大前臂血流 436 ± 38%),并且在阻断内皮一氧化氮合酶后不会被消除。He-EPC 不会影响细胞因子、粘附分子或微颗粒的血浆水平。
氦气是一种非麻醉、无毒气体,没有血液动力学副作用,可在体内诱导人类内皮的早期和晚期预处理。需要进一步的研究来确定氦气是否可以作为诱导心血管危险因素患者内皮预处理的工具。