Isoflurane induces a postconditioning effect on bovine pulmonary arterial endothelial cells exposed to oxygen-glucose deprivation.
Isoflurane induces a postconditioning effect on bovine pulmonary arterial endothelial cells exposed to oxygen-glucose deprivation.
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DOI：
10.1016/j.ejphar.2009.05.007
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发表时间：
2009-08-01
影响因子：
5
通讯作者：
Zuo Z
中科院分区：
文献类型：
--
作者：
Kim JA;Li L;Zuo Z
在再灌注开始时应用挥发性麻醉剂可减少缺血诱导的心脏和脑损伤（麻醉后处理）。本研究旨在评价挥发性麻醉药是否诱导内皮细胞的后处理效应。牛肺动脉内皮细胞（BPAEC）培养物暴露于氧-糖剥夺（一种模拟体外缺血的条件）3 h。在模拟再灌注早期应用吸入麻醉药异氟醚和地氟醚。膜联蛋白V和碘化丙啶染色后，通过乳酸脱氢酶（LDH）释放和流式细胞术测量来定量细胞损伤。氧-糖剥夺和随后的模拟再灌注增加LDH释放和膜联蛋白V阳性染色细胞，细胞凋亡的特征。后处理异氟烷，但不是地氟烷，减少这种细胞损伤。即使在再灌注开始后60分钟应用2%异氟烷，这种保护作用也是明显的。异氟烷后处理效应被格列本脲（一种一般ATP敏感性K+（KATP）通道阻滞剂）、5-羟基癸酸（一种线粒体KATP通道阻滞剂）和白屈菜红碱（一种蛋白激酶C抑制剂）消除。二氮嗪，一种线粒体KATP通道激活剂，在再灌注开始时应用，也减少了氧-葡萄糖剥夺诱导的内皮细胞损伤。白屈菜红碱和5-羟基癸酸酯可消除二氮嗪诱导的保护作用。我们的结论是，异氟烷诱导的后处理效应的BPAEC。异氟醚后处理的有效时间窗为再灌注开始后0 ~ 60 min。这种异氟醚后处理效应可能通过线粒体KATP通道和PKC介导。PKC可能是异氟烷效应的线粒体KATP通道的下游。
Application of volatile anesthetics during the onset of reperfusion reduced ischemia-induced cardiac and brain injury (anesthetic postconditioning). This study was designed to evaluate whether volatile anesthetics induced a postconditioning effect in endothelial cells. Bovine pulmonary arterial endothelial cell (BPAEC) cultures were exposed to oxygen-glucose deprivation, a condition to simulate ischemia in vitro, for 3 h. The volatile anesthetics isoflurane and desflurane were applied during the early phase of simulated reperfusion. Cell injury was quantified by lactate dehydrogenase (LDH) release and flow cytometrical measurement after annexin V and propidium iodide staining. Oxygen-glucose deprivation and the subsequent simulated reperfusion increased LDH release and annexin V-positive staining cells, a characteristic of cell apoptosis. Posttreatment with isoflurane, but not desflurane, reduced this cell injury. This protection was apparent even when 2% isoflurane was applied at 60 min after the onset of reperfusion. The isoflurane postconditioning effect was abolished by glybenclamide, a general ATP sensitive K+ (KATP) channel blocker, 5-hydroxydecanoate, a mitochondrial KATP channel blocker, and chelerythrine, a protein kinase C inhibitor. Diazoxide, a mitochondrial KATP channel activator, applied at the onset of reperfusion also decreased oxygen-glucose deprivation-induced endothelial cell injury. This diazoxide-induced protection was abolished by chelerythrine and 5-hydroxydecanoate. We conclude that isoflurane induced a postconditioning effect in BPAEC. The effective time window of isoflurane postconditioning was from 0 to 60 min after the onset of reperfusion. This isoflurane postconditioning effect may be mediated by mitochondrial KATP channels and PKC. PKC may be downstream of mitochondrial KATP channels for this isoflurane effect.
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DOI：
10.1016/0006-291x(90)91544-3
发表时间：
1990-11-15
影响因子：
3.1
作者：
HERBERT, JM;AUGEREAU, JM;MAFFRAND, JP
通讯作者：
MAFFRAND, JP
影响因子：
3.6
作者：
Zuo, ZY;Johns, RA
通讯作者：
Johns, RA
DOI：
10.1073/pnas.86.17.6758
发表时间：
1989-09-01
影响因子：
11.1
作者：
GOPALAKRISHNA, R;ANDERSON, WB
通讯作者：
ANDERSON, WB
影响因子：
37.8
作者：
MURRY, CE;JENNINGS, RB;REIMER, KA
通讯作者：
REIMER, KA
影响因子：
20.1
作者：
JABR, RI;COLE, WC
通讯作者：
COLE, WC