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机构地区:[1]暨南大学医学院病理生理教研室 [2]暨南大学医学院病发热研究室
出 处:《中国病理生理杂志》1990年第6期445-449,共5页Chinese Journal of Pathophysiology
摘 要:本研究用114只新西兰白兔进行三部分实验。1.家兔静脉注射非热限剂量、热限剂量ET引起发热时,PGE_2含量变化与体温变化之间无明显正相关(p>0.05),即ET性发热达到热限时,PGE_2含量增多不受限。2.侧脑室注射不同剂量PGEt引起的发热呈剂量一效应依赖关系,但当PGE_2剂量递增达到一定水平后,再增加剂量,发热效应不再随之增强,出现“PGE热限”。3.非热限剂量、热限剂量PGE_2引起发热时,脑脊液中cAMP含量变化与体温变化之间呈明显正相关(r=0.9906,p<0.01),PGE_2性发热达到热限水平后,cAMP含量的增多受限。作者推论:PGE可能不参与ET热限的构成,在ET性发热机制中,PGE可能不是主要的中枢介质:PGE作为致热物质也有热限存在。cAMP可能是构成PGE热限的重要介质。114 albino New Zealand rabbits were divided into three parts in this study. The results obtained were as follows: 1. The concentration of prostaglandin E_2 (PGE_2) in cerebrospinal fluid (CSF) was insignificantly correlated positively to the febrile response (r=0.8790, P>0.05) after non-fever limit (non-FL) dose and FL dose endotoxin (ET) was intravenously injected into rabbits. The increase of PGE_2 in CSF was not limited during the occurrence of ET FL. 2. Intracerebroventricular injection (ICV) of different dose of PGE_2 into rabbits induced dose-dependent fever, but there was no more rise in body temperature when the febrile response had reached a certain height. This is termed 'PGE FL'. 3. The concentration of cyclic adenosine-3′, 5′-monophosphate (cAMP)in CSF paralleled the fluctuation of temperature (r=0.9906, P<0.01) after the administration of non-FL dose and FL dose PGE_2 into rabbits. During the occurrence of PGE FL, the limitation of the increase of cAMP in CSF could be seen. On the basis of these results it is proposed that PGE is not involved in the formation of ET FL and is not an important central mediator during ET-induced fever. The cAMP may be an important factor involved in the development of PGE FL.
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