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败血症休克时心肌肌浆网Ryanodine受体的变化及其机制研究

董林旺, 吉勇, 王雪青, 吴立玲, 唐朝枢

北京医科大学心血管基础研究所休克研究室. 北京 100083

摘要

晚期败血症休克大鼠心肌肌浆网(CSR)Ryanodine与受体结合的B_(max)降低41.3%(P<0.01), Kd值无明显变化。钙离子可明显激活~(3)H-Ryanodine与其受体的结合。咖 啡因, ATP, AMP-PCP都可浓度依赖性地促进~(3)H-Ryanodine与受体的结合, 而钌 红, 氯化镁则浓度依赖性地抑制其结合。但败血症休克时上述激动剂或抑制剂的A_( 0.5)和IC_(50)均无明显改变。用磷脂酶A_(2)消化假手术动物SR后, 其~(2)H-Ryanodine与受体的结合明显降低, 将磷脂酰胆碱(PC), 磷脂酰乙醇胺(PE)和磷脂酰丝氨酸(PS) 分别参入到上述消化后的CSR膜中可明显提高~(3)H-Ryanodine与受体的低结合。同时, PC, PE, PS分别参入CSR中可显著改变败血症休克时CSR ~(3)H-Ryanodine 与受体的结 合状态。图5表1参14

关键词： 败血症休克; 膜磷脂; Ryanodine受体; 磷脂酶A_(2); 钙离子

Altered ryanodine receptor of rat cardiac sarcoplasmic reticulum and its underlying mechanism during septic shock

Dong Linwang, Ji Yong, Wang Xueqing, Wu Liling, Tang Chaoshu

Laboratory of Shock Research, Institute of Cardiovascular Research, Beijing Medical University. Beijing 100083

Abstract

Key words: Septic shock;Membrane phospholipids;Ryanodine receptor;Phospholipase A_(2); Calcium ion

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引用本文：

董林旺, 吉勇, 王雪青, 吴立玲, 唐朝枢. 败血症休克时心肌肌浆网Ryanodine受体的变化及其机制研究[J]. 生理学报 1995; 47 (4): .

Dong Linwang, Ji Yong, Wang Xueqing, Wu Liling, Tang Chaoshu. Altered ryanodine receptor of rat cardiac sarcoplasmic reticulum and its underlying mechanism during septic shock. Acta Physiol Sin 1995; 47 (4): (in Chinese with English abstract).