【摘要】 目的 :探讨清开灵 (QKL)注射液对家兔内毒素性发热的解热作用和机制。方法 :复制家兔内毒素(ET)性发热模型 ,用数字温度计测量家兔的直肠温度 ,用放免法测定下丘脑的IL - 1β和cAMP、脑脊液中的cAMP、腹中隔区的AVP含量。结果 :QKL +ET组的△T(0 2 4± 0 10 )℃、TRI1(1 0 2± 0 81)、下丘脑IL - 1β (3 0 2± 0 5 8)ng/g、下丘脑cAMP (1 37± 0 2 3)nmol/g、CSF中cAMP (14 13± 3 80 )nmol/L、腹中隔区AVP (2 5 2 4± 2 6 1)ng/g ,分别低于ET组的△T (0 4 0± 0 11)℃、TRI1(1 78± 0 79)、下丘脑IL - 1β (6 0 8± 0 79)ng/g、下丘脑cAMP (2 90± 0 4 0 )nmol/g、CSF中cAMP (32 10± 4 5 1)nmol/L、腹中隔区AVP (47 32± 3 77)ng/g ,两者相比差异显著 (P <0 0 1)。结论 :QKL抑制下丘脑内生致热原和中枢发热介质的生成 ,促进解热物质的释放 ,可能是QKL对内毒素性发热的重要解热机制。更多还原

【Abstract】 AIM: To explore the antipyretic mechanism of Qing Kai-Ling (QKL) injection on endotoxin (ET)-induced fever in rabbits. METHODS: Rabbit models of endotoxin (ET)-induced fever were duplicated. The rectal temperature was measured by digital thermograph. The cAMP and IL-1β content in the hypothalamus (HP), the cAMP content in the cerebrospinal fluid (CSF), and the arginine vasopressin (AVP) content in the ventral septal area (VSA) were determined by radioimmunoassay. RESULTS: ① QKL had significant antipyretic effect on ET-induced fever( P <0.01), ② The production of IL-1β and cAMP in HP was significantly inhibited by QKL treatment ( P <0.01), ③ QKL markedly decreased the cAMP content in the CSF and AVP content in the VSA( P <0.01). CONCLUSION: The antipyretic mechanisms of QKL are probably due to inhibiting the production of the endogenous pyrogen and central mediator of fever, and meanwhile stimulating the release of the antipyretic substances.更多还原