Isoflurane preconditioning increases endothelial cell tolerance to in-vitro simulated ischaemia.
Isoflurane preconditioning increases endothelial cell tolerance to in-vitro simulated ischaemia.
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DOI：
10.1111/j.2042-7158.2010.01198.x
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发表时间：
2011-01
期刊：
影响因子：
--
通讯作者：
Zuo Z
中科院分区：
文献类型：
--
作者：
Feng J;Zuo Z
Isoflurane preconditioning has been shown to protect endothelial cells against lipopolysaccharide and cytokines-induced injury. This study was designed to determine whether isoflurane preconditioning increased endothelial cell tolerance to ischemia. Bovine pulmonary arterial endothelial cells were exposed or not exposed to various concentrations of isoflurane for 1 hr. After a 30-min isoflurane-free period, cells were subjected to oxygen-glucose deprivation (OGD) for 3 hr and reoxygenation for 1 hr. Lactate dehydrogenase (LDH) release from cells was used to measure cell injury. In some experiments, various protein kinase C (PKC) inhibitors and ATP-sensitive potassium channel (KATP channel) inhibitors were present from 30 min before isoflurane treatment to the end of isoflurane treatment. Isoflurane preconditioning dose-dependently decreased the OGD-induced LDH release. This protection was inhibited by 2 μM chelerythrine, a general PKC inhibitor, or 10 μM GÖ6976, an inhibitor for the conventional PKCs. This protection also was inhibited by 0.3 μM glybenclamide, a general KATP channel inhibitor, and 500 μM 5-hydroxydecanoate, a mitochondrial KATP channel blocker. In addition, pretreatment with 100 μM diazoxide, a KATP channel activator, for 1 hr also reduced OGD-induced endothelial cell injury. This diazoxide-induced protection was inhibited by chelerythrine. Our results suggest that isoflurane preconditioning induces endothelial protection against in vitro simulated ischemia. This protection may be mediated at least in part by conventional PKCs and mitochondrial KATP channels. Our results also indicate that PKCs may be downstream of KATP channels in causing endothelial protection.
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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