吗啡后处理对大鼠心肌细胞ATP敏感性钾通道的影响  

Effect of Morphine Postconditioning on Rat Cardiac Sarcolemmal KATP Channels

作　　者：唐贞申[1] 钮伟真[2] 魏华[2] 李天佐[1] 刘萍[2] 张炳熙[1] 

机构地区：[1]首都医科大学附属北京同仁医院麻醉科,北京100730 [2]首都医科大学生理学教研室,北京100069

出　　处：《生物化学与生物物理进展》2009年第12期1562-1568,共7页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金资助项目(30672023)~~

摘　　要：在氰化钠(NaCN)处理模拟细胞缺血的单个大鼠心肌细胞上,应用膜片钳电压钳制全细胞记录模式,研究吗啡后处理对缺血心肌细胞膜ATP敏感性钾通道的影响,并探讨吗啡后处理可能涉及的阿片受体类型.吗啡后处理可使ATP敏感性钾通道电流(IKATP)增加(61.4±13.6)%,促进KATP通道开放.特异阻断κ-阿片受体不能阻止IKATP增加,而非特异性阻断阿片受体或特异阻断δ-阿片受体均可阻止IKATP增加.结果表明,吗啡后处理促进KATP通道开放与δ-阿片受体的激活有关.The KATP channel current （IKATP） was monitored using the whole cell configuration of the patch clamp technique in single ventricular cardiac myocytes enzymatically isolated from rat hearts. Sodium cyanide, a metabolic inhibitor, was used to mimic cell ischemia. Morphine postconditioning facilitated the further opening of the KATP channels. Following initial activation of IKATP by mimic ischemia, morphine further increased current amplitude by （61.4 ±13.6）%. KATP channels in normal cardiac myocytes were not affected by extracellular applications of morphine alone. Nor-binaltorphimine, a specific κ-opioid receptor antagonist, was unable to abolish the facilitation of morphine postconditioning when administered 5 minutes before morphine. However, naloxone, a non-specific opioid receptor antagonist, and naltrindole, a specific δ-opioid receptor antagonist, can abolish the facilitation of morphine postconditioning. These results indicated that morphine postconditioning facilitate the further opening of the cardiac sarcolemmal KATP channels following the channel activation by mimic ischemia. The δ-opioid receptor may be involved in morphine postconditioning.

关 键 词：膜片钳 心肌细胞 模拟缺血 吗啡后处理 ATP敏感性钾通道 

分 类 号：R614[医药卫生—麻醉学]