摘要
为确定cAMP和PGE是否参与EGTA性发热的机制,作者用40只家兔进行实验,观察预先静脉灌注一定剂量水杨酸钠对侧脑室灌注EGTA所引起的发热效应以及脑脊液cAMP和PGE_2含量的增多有何影响。实验结果表明:静脉注射1.25mM随后以9.6μM/分钟恒速灌注水杨酸钠,可抑制由侧脑室灌注0.6mM EGTA所引起的脑脊液PGE_2含量增多(P<0.01),但对其引起的发热效应及脑脊液cAMP含量增多无明显影响(P>0.05),在EGTA性发热时,发热效应与脑脊液cAMP含最增多之间呈明显正相关(r=0.983 9,P<0.01)。据此,作者推论:在EGTA性发热机制中,中枢Na^+/Ca^(++)比值增高引起cAMP含量增多可能起重要作用;而中枢PGE_2含量增多则不是必需环节,也不是中枢cAMP含量增多的原因。
In order to determine further whether cAMP and PGE takes part in the mechanism of EGTA-induced fever in the present experiment with 40 New Zealand rab bits, the influence of intravenous infusion of sodium salicylate (SS) on the febrile response and the rise of cAMP and PGE_2 concentration in c.s.f. produced by intraventricular perfusion of EGTA were observed. The results showed that intravenous infusion of SS (9.6μM/min. following an initial dose of 1.25mM) could inhibit the rise of PGE_2 concentration in c.s.f. (P<0.01), but could not inhibit the rise of rectal temperature and cAMP concentration in c.s.f. (P>0.05) after 0.6 mM EGTA was perfused into lateral cerebroventricle. The concentration of cAMP in c.s.f. was correlated apparently positively with the febrile response in EGTA-induced fever (r=0.9839, P<0.01). On the bases of these results, This is suggested that in the mechanism of EGTA-induced fever, the rise of cAMP concentration in CNS may be an improtant factor, while PGE in CNS is neither an essential mediator nor the cause leading to the rise of cAMP concentration in CNS.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第5期461-465,共5页
Chinese Journal of Pathophysiology
基金
广东省科委科学基金
关键词
发热
钠
钙
水杨酸钠
脑脊液
Fever
Sodium
Calcium
Adenosine cyclic monophosphate
Prostaglandins E