Clinic of Anesthesiology, Ludwig-Maximilians-University Munich, Munich, Germany.
Anesthesiology. 2011 Sep;115(3):483-91. doi: 10.1097/ALN.0b013e3182289988.
Adhesion of polymorphonuclear neutrophils and platelets to the vessel wall contributes to generating ischemia-reperfusion injury. Endothelial adhesion molecules are harbored within the glycocalyx, which covers every healthy vascular endothelium but is deteriorated by ischemia-reperfusion. Pretreating the heart with volatile anesthetics reduces myocardial infarct size and protects against ischemia-reperfusion injury. The authors analyzed a possible protective effect of sevoflurane on the glycocalyx and implications for postischemic cell adhesion.
Isolated guinea pig hearts were perfused with crystalloid buffer and subjected to 20 min of global warm ischemia and 10 min of reperfusion. An intracoronary bolus of 3 x 10(6) polymorphonuclear neutrophilic leukocytes or 1 x 10(9) platelets of human origin was applied after reperfusion, either with or without pretreating with 0.5 or 1 minimal alveolar concentration sevoflurane. The number of sequestered cells was calculated from the difference between coronary input and output. Coronary effluent was collected throughout reperfusion to measure shedding of the glycocalyx.
Ischemia-reperfusion induced a significant increase in median (interquartile range) adhesion versus control nonischemic hearts of both leukocytes (38.9 (36.3-42.9) vs. 14.5 (13.1-16.0)%) and platelets (25.0 (22.5-27.1) vs. 9.4 (8.4-10.7)%). Shedding was evidenced by eightfold increases in washout of syndecan-1 and heparan sulfate versus basal. Sevoflurane reduced cell adhesion to near basal at 1 minimal alveolar concentration (leukocytes: 21.2% (19.2-23.9%), platelets: 11.5% (10.4-12.0%). Shedding measurements and electron microscopy demonstrated that sevoflurane-treated hearts retained much of their 200 nm-thick glycocalyx.
Sevoflurane reduces glycocalyx shedding in the postischemic coronary bed, maintaining the natural cover for endothelial adhesion molecules and, thus, reducing cell adhesion. This may explain beneficial outcomes linked to clinical use of volatile anesthetics after ischemia-reperfusion.
多形核白细胞和血小板与血管壁的黏附有助于产生缺血再灌注损伤。内皮黏附分子存在于糖萼内，糖萼覆盖着每一个健康的血管内皮，但会因缺血再灌注而受损。用挥发性麻醉剂预处理心脏可减少心肌梗死面积并防止缺血再灌注损伤。作者分析了七氟醚对糖萼的可能保护作用及其对缺血后细胞黏附的影响。
用晶体缓冲液灌注分离的豚鼠心脏，进行 20 分钟的全温缺血和 10 分钟的再灌注。再灌注后，通过冠状动脉内推注 3×10^6 个源自人类的多形核中性粒细胞或 1×10^9 个血小板，无论是否预先用 0.5 或 1 个最小肺泡浓度的七氟醚预处理。从冠状动脉输入和输出之间的差异计算被隔离的细胞数量。整个再灌注过程中收集冠状流出物以测量糖萼的脱落。
缺血再灌注导致白细胞（38.9（36.3-42.9）%比非缺血对照心脏增加 38.9（36.3-42.9）%）和血小板（25.0（22.5-27.1）%比非缺血对照心脏增加 25.0（22.5-27.1）%）的黏附显著增加。通过 syndecan-1 和硫酸乙酰肝素冲洗量增加 8 倍来证明糖萼脱落，与基础值相比。七氟醚将细胞黏附降低至接近基础水平（1 个最小肺泡浓度时白细胞：21.2%（19.2-23.9%），血小板：11.5%（10.4-12.0%））。脱落测量和电子显微镜显示，七氟醚处理的心脏保留了大部分 200nm 厚的糖萼。
七氟醚可减少缺血后冠状动脉床中糖萼的脱落，维持内皮黏附分子的天然覆盖，从而减少细胞黏附。这可能解释了与缺血再灌注后临床使用挥发性麻醉剂相关的有益结果。
