INTERLEUKIN-1 CONTRIBUTES TO THE INDUCTION OF NITRIC-OXIDE SYNTHASE BY ENDOTOXIN IN-VIVO

被引:84
作者
SZABO, C [1 ]
WU, CC [1 ]
GROSS, SS [1 ]
THIEMERMANN, C [1 ]
VANE, JR [1 ]
机构
[1] ST BARTHOLOMEWS HOSP, COLL MED, WILLIAM HARVEY RES INST, CHARTERHOUSE SQ, LONDON EC1M 6BQ, ENGLAND
关键词
ENDOTOXIN SHOCK; VASODILATATION; VASCULAR HYPOREACTIVITY; CIRCULATORY SHOCK; CYTOKINE;
D O I
10.1016/0014-2999(93)90634-T
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
We investigated the role of interleukin-1 in the induction of a Ca2+-independent nitric oxide (NO) synthase by bacterial endotoxin in vivo. In anaesthetized rats, pretreatment with interleukin-1 receptor antagonist (interleukin-1ra; 16 mg kg-1 i.v.. followed by an infusion of 2.4 mg kg-1 h-1) ameliorated the delayed hypotension and tachycardia in response to endotoxin (2 mg kg-1 i.v.). Endotoxaemia for 3 h induced a Ca2+-independent NO synthase activity in the lung and reduced the contractions to noradrenaline in the thoracic aorta ex vivo. Treatment with interleukin-1ra attenuated both the induction of NO synthase in the lung (by 46 +/- 5%) and the endotoxin-induced hyporeactivity to noradrenaline in the aorta. Thus, endogenous interleukin-I contributes to the induction of NO synthase in response to endotoxin in vivo.
引用
收藏
页码:157 / 160
页数:4
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