Laboratory of Animal Physiology, School of Biology, Aristotle University of Thessaloniki, Thessaloníki, Greece.
Mol Cell Biochem. 2014 Mar;388(1-2):195-201. doi: 10.1007/s11010-013-1910-5. Epub 2013 Nov 26.
According to a compelling body of evidence anesthetic preconditioning (APC) attenuates the deleterious consequences of ischemia-reperfusion and protects the heart through a mechanism similar to ischemic preconditioning. The present study was purported to investigate the intracellular signaling pathways activated in human myocardium in response to a preconditioning protocol with two different volatile anesthetics, namely isoflurane and sevoflurane. To this aim, phosphorylation of PKCα and -δ, ERK1/2, Akt, and GSK3β was determined at the end of the APC protocol, in human atrial samples harvested from patients undergoing open-heart surgery. The results demonstrate that preconditioning with volatile anesthetics triggers the activation of PKCδ and -α isoforms and of prosurvival kinases, ERK1/2, and Akt, while inhibiting their downstream target GSK3β during the memory phase.
大量证据表明,麻醉预处理 (APC) 通过类似于缺血预处理的机制减轻了缺血再灌注的有害后果,并保护了心脏。本研究旨在研究在两种不同挥发性麻醉剂(即异氟烷和七氟烷)的预处理方案作用下,人类心肌中被激活的细胞内信号通路。为此,在接受心脏直视手术的患者的心房样本中,在 APC 方案结束时确定 PKCα 和 -δ、ERK1/2、Akt 和 GSK3β 的磷酸化。结果表明,挥发性麻醉剂预处理会触发 PKCδ 和 -α 同工型以及生存促进激酶 ERK1/2 和 Akt 的激活,同时在记忆阶段抑制其下游靶标 GSK3β。