摘要
目的：观察α－黑素细胞刺激素（α－ＭＳＨ）拮抗剂［Ｄ－Ｔｒｐ７，Ａｌａ８，Ｄ－Ｐｈｅ１０］α－ＭＳＨ（６－１１）－ａｍｉｄｅ对家兔内毒素（ＥＴ）及肿瘤坏死因子（ＴＮＦ）性发热的影响。方法：侧脑室给药，ＳＴ－１型数字温度计测家兔的结肠温度。结果：（１）静脉注射ＥＴ，家兔体温呈典型的双相热；若事先侧脑室注射α－ＭＳＨ拮抗剂，则体温升高更明显，且热程明显延长，６ｈ体温反应指数（ＴＲＩ６）显著高于ＮＳ＋ＥＴ组（Ｐ＜０．０１）。（２）侧脑室注射ＴＮＦ－α引起体温明显升高；事先给予α－ＭＳＨ拮抗剂，则显著增强ＴＮＦ－α性发热效应（Ｐ＜０．０１）。而α－ＭＳＨ拮抗剂对正常体温无影响。结论：内源性解热物质α－ＭＳＨ在限制发热中发挥了重要作用。
AIM: To observe the effect of α-MSH antagonist [D-Trp 7,Ala 8,D-Phe 10 ]α-MSH(6-11)-amide on fever induced by endotoxin(ET) and tumour necrosis factor-α(TNF-α).METHODS: α-MSH antagonist was injected into a lateral cerebral ventricle of rabbits. Colonic temperature was measureed with thermistor probes. RESULTS: (1) Intravenous injection of ET caused fever with biphasic thermal response. Pretretment with [D-Trp 7,Ala 8,D-Phe 10 ]α-MSH(6-11)-amide significantly enhanced and prolonged the febrile response to ET. Colonic temperature remained elevated through 6h recording period. (2) Intracerebroventricular injection of TNF-α produced the rise in temperature. [D-Trp 7,Ala 8,D-Phe 10 ]α-MSH(6-11)-amide markedly increased TNF-α-induced fever but did not alter normal temperature. CONCLUSION: Endogenous central α-MSH contributes to physiological limitation of fever.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第5期423-425,共3页
Chinese Journal of Pathophysiology
关键词
发热
内毒素
肿瘤坏死因子
Α-MSH
Fever
Endotoxins
Tumor necrosis factor
Melanocyte-stimulating hormone
