摘要
休克时糖皮质激素受体的变化及大剂量糖皮质激素抗休克治疗的受体机制△徐仁宝（第二军医大学病理生理教研室，上海２００４３３）ＡｂｓｔｒａｃｔＷｉｔｈｒａｄｉｏｌｉｇａｎｄｂｉｎｄｉｎｇａｓａｙａｎｄＳｃａｔｃｈａｒｄａｎａｌｙｓｉｓｉｔｈａｓｂｅｅｎｄｅ...
With radioligand binding assay and Scatchard analysis it has been demonstrated that both the binding capacity and the affinity of GR were reduced after stress and shock in rats,dog and in patients with hemorrhagic shock,toxic shock,and multiple organ failure.When endotoxin was injected to GRblocked rats,the pathological changes were much more severe as compared with the rats injected with endotoxin only without GR blockade.Similar results have been obtained also in GRblocked rats after hemorrhage.Thus it may be concluded that GR decrease may be implicated in the pathogenesis of shock and SIRS.GR may be downregulated by GC,so the increased secretion of GC is responsible for the reduction of GR in stress and shock,but some experimental evidences suggested heat shock response(HSR)may be alternative mechanism.We have demonstrated the existence of low affinity GR(GRL)in the target cells of GC by Scatchard analysis.We hypothesized that the therapeutic effect of GC should be mediated by GRL,if GR decreased markedly,this might be the reason why massive dose of GC is required under severe stress conditions in spite of the high concentration of plasma GC.
出处
《基础医学与临床》
CSCD
1998年第1期5-10,4,共7页
Basic and Clinical Medicine
基金
国家自然科学基金
关键词
休克
糖皮质激素
受体
药物疗法
感染性休克
glucocorticoids glucocorticoid receptor shock SIRS endotoxemia hemorrhage rats
