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离子载体A23187诱导血浆蛋白渗漏的机制及其被吲哚美辛抑制的机制。

Mechanism of ionophore A23187 induction of plasma protein leakage and of its inhibition by indomethacin.

作者信息

Thomas G

出版信息

Eur J Pharmacol. 1982 Jun 16;81(1):35-42. doi: 10.1016/0014-2999(82)90598-2.

DOI:10.1016/0014-2999(82)90598-2
PMID:6180911
Abstract

Calcium ionophore A23187 produced a dose-dependent increase in plasma protein leakage on intradermal injection in rats. Studies with mepyramine and cyproheptadine indicated that histamine and 5-hydroxytryptamine (5-HT) partially contribute to the ionophore action and experiments with compound 48/80 supported these findings. Depletion of plasma kininogen levels with cellulose sulphate administered indomethacin inhibited the ionophore response in a dose-dependent manner. The inhibition was not reversed by intradermally injected prostaglandin E2 (PGE2) in doses up to 50 ng/site, suggesting that PGE2 also may not be an important mediator. It is proposed that the ionophore produces plasma protein leakage by an indirect (through histamine and 5-HT release) and a direct action on vascular endothelial cells and that indomethacin antagonises both actions by inhibiting calcium transport processes.

摘要

钙离子载体A23187在大鼠皮内注射时可引起剂量依赖性的血浆蛋白渗漏增加。用美吡拉敏和赛庚啶进行的研究表明,组胺和5-羟色胺(5-HT)部分介导了离子载体的作用,用化合物48/80进行的实验支持了这些发现。用硫酸纤维素给予消炎痛使血浆激肽原水平降低,以剂量依赖性方式抑制了离子载体反应。皮内注射高达50 ng/部位的前列腺素E2(PGE2)不能逆转这种抑制作用,提示PGE2可能也不是重要的介质。有人提出,离子载体通过间接作用(通过组胺和5-HT释放)以及对血管内皮细胞的直接作用导致血浆蛋白渗漏,而消炎痛通过抑制钙转运过程拮抗这两种作用。

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Histamine type I receptor occupancy increases endothelial cytosolic calcium, reduces F-actin, and promotes albumin diffusion across cultured endothelial monolayers.组胺I型受体占有率增加内皮细胞胞质钙,减少F-肌动蛋白,并促进白蛋白跨培养的内皮单层扩散。
J Cell Biol. 1986 Dec;103(6 Pt 1):2379-87. doi: 10.1083/jcb.103.6.2379.
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The effects of indomethacin and verapamil on the shape changes of vascular endothelial cells resulting from exposure to various inflammatory agents.
吲哚美辛和维拉帕米对暴露于各种炎性介质下血管内皮细胞形态变化的影响。
Agents Actions. 1988 Jul;24(3-4):351-5. doi: 10.1007/BF02028293.
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