摘要
为探索细胞介素ＴＮＦ－α升体温效应与下丘脑前部、视前区（ＰＯＡＨ）中的阿片受体的关系。应用脑神经核团微量注射方法给自由状态下的雄性ＳＤ大鼠ＰＯＡＨ区微量注射ＴＮＦ－α致热源。给药前３０ｍｉｎ分别用通常阿片受体拮抗剂Ｎａｌ（１０～２０μｇ）和特异性阿片受体μ、δ和κ的拮抗剂ＣＴＡＰ（１．０～２．５μｇ）、ＮＴＩ（０．２５～０．５μｇ）和ｎｏｒ－ＢＮＩ（０．１～３μｇ）对ＰＯＡＨ做预处理。结果：单独给ＴＮＦ－α可致剂量相关的体温升高△Ｔ（１℃～１．４℃）；经Ｎａｌ１０μｇ，ＣＴＡＰ１．０μｇ和ＮＴＩ０．５μｇ处理后使ＴＮＦ－α的升体温效应减弱；用Ｎａｌ２０μｇ，ＣＴＡＰ２．５μｇ和ＮＴＩ０．２５μｇ处理后可完全阻断ＴＮＦ－α所致的体温升高；ｎｏｒ－ＢＮＩ（０．１～３μｇ）对ＴＮＦ－α的升体温效应无影响。
he present study is to define Interaction between cytokine TNF α induced hyperthermia and opioid receptors in the POAH. TNF α(5～40 ng)was injected into the POAH of male unrestrained S D rat by the method of the brain neucli microinjection to select a pyrogen dose induced hyperthermia. 30 minutes prior to the injection of pyrogen, the POAH of experimental groups were pre treated with general opioid receptor antagonists Nal(10～20 μg), Selective μ,δ,κ receptor antagonists CTAP(1～2.5μg), NTI(0.25～0.5 μg )and nor BNI(0.1～3 μg) respectively. Results: TNF α(5～40 ng) induced a dose dependent hyperthermia (ΔT:1 ～1.4℃);Hyperthermia caused by TNF α(10ng) was reduced by Nal(10 μg), CTAP(1.0 μg) and NTI (0.5 μg); and completely blocked by Nal(20 μg),CTAP(2.5 μg) and NTI(0.25 μg); nor BNI(0.1～3 μg)did not affect TNF α indued hyperthermia. [WT5”HZ〗
出处
《中国医科大学学报》
CAS
CSCD
1996年第6期579-581,604,共4页
Journal of China Medical University
基金
国家自然科学基金
美国NIDA基金
中华医学基金
