This study investigates the role of extracellular brain calcium in the hyperthermia induced by interleukin-1 beta (IL-1 beta). 2. Intracerebroventricular (i.c.v.) injection of IL-1 beta (12.5 ng kg-1) in rabbits caused a prompt and sustained rise in cerebrospinal fluid (CSF) Ca2+ concentration ([Ca2+]) followed by enhanced prostaglandin E2 (PGE2) release and hyperthermia. 3. A linear and significant correlation was observed between the increase in [Ca2+] induced by IL-1 beta and the rise in body temperature. 4. Ventriculo-cisternal perfusion with artificial CSF containing the calcium chelator EGTA (1.3 mM) blocked the IL-1-induced PGE2 release and countered the febrile response. 5. I.c.v. administration of dexamethasone (Dex) (2.4 and 24 micrograms kg-1) 100 min prior to IL-1 beta, dose-dependently antagonized the cytokine-induced Ca2+ increase, the PGE2 release and the febrile response. 6. These results suggest that changes in extracellular brain calcium are involved in the regulation of body temperature. In this light, the antipyretic action of Dex may be related to its effect on Ca2+ uptake.
摘要
本研究调查细胞外脑钙在白细胞介素-1β（IL-1β）诱导的体温过高中的作用。2. 给家兔脑室内（i.c.v.）注射IL-1β（12.5 ng kg-1）导致脑脊液（CSF）中Ca2+浓度（[Ca2+]）迅速且持续升高，随后前列腺素E2（PGE2）释放增加以及体温过高。3. 观察到IL-1β诱导的[Ca2+]升高与体温升高之间存在线性且显著的相关性。4. 用含钙螯合剂乙二醇双四乙酸（EGTA，1.3 mM）的人工脑脊液进行脑室-脑池灌注可阻断IL-1诱导的PGE2释放并对抗发热反应。5. 在注射IL-1β前100分钟脑室内给予地塞米松（Dex）（2.4和24微克 kg-1），剂量依赖性地拮抗细胞因子诱导的Ca2+增加、PGE2释放和发热反应。6. 这些结果表明细胞外脑钙的变化参与体温调节。据此，Dex的解热作用可能与其对Ca2+摄取的影响有关。
