摘要
本文用30只封闭群新西兰白色家兔进行两部分试验。第一部分:观察侧脑室内注射TNF的发热效应;第二部分:用放免法检测TNF发热高峰时血浆和脑脊液中PGE_2和cAMP的含量。实验结果显示:侧脑室内注射50ng/只TNF(rTNF组)可引起家兔发热达△T0.79±0.14℃。此时:(1)脑脊液中PGE_2水平明显高于对照组(注射同量生理盐水)(2)血浆中PGE_2含量与对照组无显著差别。上述结果表明:①侧脑室内注射rTNF可在外周血PGE_2不增多的情况下引起脑内PGE_2合成增加。②PGE_2的升高并未引起cAMP的升高。从而提示TNP与白细胞致热原(LP或IL-1)在引起发热的机制上可能有不同方式,PGE_2升高可能参与TNF性发热的机制,不支持PGF_2升高通过cAMP升高引起发热的主张。
Thirty New Zealand albino rabbits of both sexes were used for the experi-ments which was (1) To observe the febrile response induced by microinjection of TNFinto the lateral ventricle; (2) To measure the PGE_2 & cAMP contents of the plasma andcerebrospinal fluid. The results showed that injection of TNF (50ng/each) into the lateralventricle did induce a definite raise of body temperature (T=0.79±0.14℃). The PGE_2concentration increased markedly in c. s. f. while that in plasma remain unchanged ascompared with the control. However cAMP lever in both, plasma and c. s. f. had nochange. These results suggested that (1) The injection of TNF into the lateral ventriclecaused a raise in PGE_2 synthesis in the brain while there was no alterations of PGE_2found in peripheral blood (2) The increase in PGE_2 didn't followed by an increase incAMP which indicated that the fever induced by TNF must have a different mechanismfrom that induced by leucocyte pyrogent (LP or In-1). PGE_2 might be involved in thefever inducing mechanism but these results don't support the hypothersis that the raiseof PGE_2 level may increase the cAMP content which in turn reduced the fever.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1993年第2期165-169,共5页
Chinese Journal of Pathophysiology
关键词
肿瘤坏死因子
发热
前列腺素
Tumor necrosis factor
Fever
Prostaglandins E
Adenosine cyclic monophosphate
