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Mechanism of low K+ buffer aggravating reperfusion injury in rat ventricular myocytes
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- Author:
- No author available
- Journal Title:
- JOURNAL OF THE FOURTH MILITARY MEDICAL UNIVERSITY
- Issue:
- 23
- DOI:
- 10.3321/j.issn:1000-2790.2006.23.005
- Key Word:
- 低钾;钠-钙交换体;钙震荡;心肌细胞
Abstract： 目的:观察低钾灌流液对大鼠心肌细胞再灌注时钙震荡的影响并探讨其作用机制. 方法:Ca2+荧光指示剂Fura-2标记心肌细胞,在代谢抑制并低氧25 min后,改用低钾台氏液([K+]=3.0 mmol/L)灌流,记录细胞钙震荡的变化. 以(再灌注末期细胞长度-缺血末期细胞长度)/(缺血前细胞长度-缺血末期细胞长度)×100%反映再灌注后细胞长度的恢复状况. 结果:与含正常钾浓度的灌流液对照组([K+]=5.4 mmol/L)相比,在再灌注10 min内,低钾灌流液组出现钙震荡的次数显著增加(P＜0.01,低K+组:138.80±9.54 vs对照组:82.30±8.16,n=6),心肌细胞长度的恢复显著被抑制[P＜0.01,低K+组:(24.30±6.01)% vs对照组:(54.50±6.56)%,n=6];再灌注期间给予钠-钙交换体反向交换模式抑制剂KB-R7943,可显著抑制低钾溶液对钙震荡和细胞长度的影响[P＜0.01 vs低K+组,n=6; 钙震荡:27.40±6.76和细胞长度恢复:(58.90±7.30)%]. 结论:低钾再灌注液通过增强反向钠-钙交换体活性加重钙震荡,进而引发心肌损伤.
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