缺血预适应对缺氧复氧后细胞离子稳态的影响及机制

研究缺血预适应对大鼠心肌细胞缺氧 复氧后离子稳态的影响及可能机制以及探讨缺血预适应抗心律失常的离子基础。采用Langdorff逆行灌流技术分离SD大鼠心肌细胞。按①缺血预适应组、②Glibenclamide干预缺血预适应组、③哇巴因 (OUB)干预缺氧 复氧组、④缺氧 复氧组、⑤Cromakalim(CRK)干预缺血预适应组、⑥OUB和CRK干预缺氧 复氧组、⑦正常对照组 ,分组孵育细胞 ,观察缺血预适应对缺氧 复氧后心肌细胞内钠、钾离子水平 ,细胞膜Na+ K+ ATP酶 (Na+ K+ ATPase)活性的影响。结果 :与单纯缺氧 复氧相比 ,缺血预适应使心肌细胞乳酸脱氢酶(LDH)漏出量下降 (2 1.75± 7.2 9vs 89.6 3± 2 4IU) ;同时维持Na+ K+ ATPase活性在较高水平 (6 .42± 0 .8vs 3 .18±0 .6 2 μmol·mg-1·h-1) ,保持细胞内较高的钾离子水平 (386 .5± 83vs 10 7.5± 2 9.96 μg/mg)和较低的钠离子水平(372 .5± 5 7.2 7vs 5 6 3 .0 7± 94.0 2 μg/mg)。此效应可被OUB及ATP敏感性钾通道阻滞剂Glibendamide所阻断。结论 :缺血预适应促进ATP敏感性钾通道的开放 ,减轻细胞膜损伤 ,维持细胞核Na+ K+ ATPase在较高水平 ,从而减少了缺氧 复氧后钠超载 ,增加了钾离子的再摄取 ,可能是缺血预适应稳定离子稳态的机制。细胞内外离子稳态的形成可?

Effect of Ischemia Preconditioning on Ions Homeostasis of Anoxic Reoxygenated Cardiomyocytes of SD Rats.

The aim of the paper is to investigate the effect of ishchemic preconditioning (PC) on ion homeostasis of isolated cardiomyocytes,and discuss its ion basis of antiarrythmis.Isolated cardiomyocytes were used to study the effect of PC on the cellular concentration of K +,Na +,and the activity of Na + K + ATP ase .Isolated cardiomyocytes were divided into 7 groups.GroupⅠ=PC;GroupⅡ=PC+Glibenclamide(GLB);GroupⅢ=PC+Ouabain(OUB);GroupⅣ=anoxic reoxygenated (AR);GroupⅤ=Cromakalim(CRK)+AR;GroupⅥ=OUB+CRK+AR;GroupⅦ=Control.Results: From anoxic reoxygenated cycle 1 to 2 and 3,concentration of extracellular potassium increased gradually which could be block by GLB.After exposure to anoxic reoxygenated,the activity of Na + K + ATP ase in Group Ⅰ was maintained at higher level (6.42±0.8 μmol·mg -1 ·h -1 ) with higher intracellular potassium concentration (386.5±83.33 μg/mg) and lower intracellular sodium concentration (372.5±57.27 μg/mg).GLB blocked the protective effect of PC in Group Ⅱ with lower activity of Na + K + ATP ase (3.62±0.96 μmol·mg -1 ·h -1 ) and higher intracellular sodium concentration 518.67±61.18 mg.protein/hr),OUB also blocked the protective effect of PC with lower activity of Na + K + ATP ase (1.61±0.57 μmol·mg -1 ·h -1 ),lower intracellular potassium concentration (87.67±18 μg/mg) and higher intracellular sodium concentration (732.54±54.4 μg/mg).The leakage of LDH had a corresponding change with the activity of Na + K + ATP ase .Conclusion:PC promoted the opening of ATP sensitive potassium channel and alleviated the cellular injury,in turn maintained the activity of ATP sensitive of Na + K + ATP ase and ion homeostasis.It may be one of the mechanisms of PC suppressing arrhythmias.Chinese Journal of Cardiac Pacing and Electrophysiology,2000,14(3):191～194]