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为探讨内毒素(ET)和内生致热原(EP)热限的机制,在家兔静脉注射非热限与热限剂量的EF或EP后及热限加不同致热原负荷时,用竟争性蛋白结合法检测脑脊液和血浆样品中cAMP的含量。结果发现:(1).脑脊液中cAMP含量随EF性发热效应的增强而升高,到达EP热限后则不再上升,而血浆cAMP含量无类似变化。(2).脑脊液和血浆中cAMP含量均随ET性发热效应的增强而上升,到达ET热限后均不再升高。(3).虽然ET热限的发热水平明显高于EP热限,且EP热限加ET负荷使发热水平超过EP热限;但各组之间脑脊液中cAMP含量却无明显差异。上述结果表明,中枢cAMP生成受限可能既是构成EP热限的重要因素,又是ET热限的一个重要成因。但是除cAMP外,ET热限的构成还与其它因素有关。
In order to explore the mechanism of endotoxin (ET) and endogenous pyrogen (EP) heat limit, after intravenous injection of non-heat-limited and heat-limited doses of EF or EP, Competitive protein binding assay for cAMP in cerebrospinal fluid and plasma samples. The results showed that: (1) The cAMP content in cerebrospinal fluid (CSF) increased with the enhancement of EF febrile sequelae, but no longer increased after reaching the EP heat limit, while the plasma cAMP content showed no similar changes. (2) The contents of cAMP in cerebrospinal fluid (CSF) and plasma increased with the increase of ET fever, and no increase after reaching ET heat limit. (3) Although ET fever limit fever was significantly higher than the EP heat limit, and EP heat load plus ET load so that the fever level exceeded the EP heat limit; but there was no significant difference in cAMP content between cerebrospinal fluid in each group. The above results indicate that the limitation of central cAMP generation may be both an important factor for forming the EP thermal limit and an important cause for the ET thermal limit. However, in addition to cAMP, the composition of the ET heat limit is also related to other factors.