钙离子激活的钾离子外流与缺血性脑水肿的形成有关吗？

Is Ca2+ -activated potassium efflux involved in the formation of ischemic brain edema?

作者信息

Tominaga T, Katagi H, Ohnishi S T

机构信息

Membrane Research Institute, University City Science Center, Philadelphia, PA 19104.

出版信息

Brain Res. 1988 Sep 20;460(2):376-8. doi: 10.1016/0006-8993(88)90385-x.

DOI:10.1016/0006-8993(88)90385-x

PMID:2465063

Abstract

A possible role of Ca2+ -activated potassium efflux in brain ischemia was studied using a rat focal cortical infarction model. Three days after ischemic insult, tissue contents of water, sodium, potassium and calcium ions were measured. Charybdotoxin, a specific inhibitor of Ca2+ -activated potassium efflux, was found to reduce the formation of ischemic brain edema when a dosage of 0.15 mg/kg was given by i.v. 20-30 min prior to the onset of ischemic insult.

摘要

利用大鼠局灶性皮质梗死模型研究了Ca2+激活的钾外流在脑缺血中的可能作用。缺血损伤三天后，测量水、钠、钾和钙离子的组织含量。发现大剂量毒素（一种Ca2+激活的钾外流特异性抑制剂）在缺血损伤开始前20 - 30分钟静脉注射0.15 mg/kg剂量时，可减少缺血性脑水肿的形成。