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首页> 外文期刊>Journal of Medical Colleges of PLA >Effect of simulated ischemia- reperfusion on I_f in sinoatrial node cells and the intervention of KATP channel opener
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Effect of simulated ischemia- reperfusion on I_f in sinoatrial node cells and the intervention of KATP channel opener

机译:模拟缺血再灌注对窦房结细胞I_f的影响及KATP通道开放剂的干预

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摘要

Objective: To study the effect of simulated ischemia-reperfusion (I/R) on I_f of sinoatrial node (SAN) cells and the intervention of KATP channel opener Pinacidil. Methods: The SAN cells of the neonatal rats were detached and purified 2 d before the experiment. The experimental animals were randomly divided into the control group, group of simulated I/R, group intervened with KATP channel opener Pinacidil (P+ I/R) and group intervened with KATP channel blocking agent 5-HD (5-HD + P + I/R & 5-HD + I/R) . The I_f density of each group was measured by technique of routine whole cell patch clamp and multiple- catheter perfusion system and the I_f activated curve in each group was drawn. Results: ①Under different directive potentials, the I_f density of the SAN cells in I/R group increased significantly, compared with that in the control group ( P < 0.01) ; that in P + I/R group decreased significantly, compared with that in I/R group ( P < 0.01 ); the I_f density values in 5-HD + P + I/R group and 5-HD + I/R group increased significantly, compared with that in P + I/R group, but showed no significant difference with that in I/R group. ②Compared with that in the control group, the I_f activated curve of the SAN cells moved rightwards under ultimate activating potential, half of which was from - 108.0 +- 12.4 to - 89.5 +- 7.2 mV ( P < 0.01 ); compared with that in I/R group, I_f activated curve of the SAN cells moved leftwards under ultimate activating potential, half of which was the range from - 99. 5 +- 10. 8 mV ( P < 0.05); KATP channel blocking agent 5-HD could block the effect of Pinacdil on I_f activated curve. Conclusion: KATP channel opener Pinacidil can antagonize the effect of simulated I/R on the I_f of SAN cells, which may be beneficial to the maintenance of the relative stability of ion steady state and electrophysiological activities under condition of simulated I/R.
机译:目的:研究模拟缺血再灌注(I / R)对窦房结(SAN)细胞I_f的影响以及KATP通道开放剂Pinacidil的干预作用。方法:实验前2 d,分离纯化新生大鼠SAN细胞。实验动物随机分为对照组,模拟I / R组,干预KATP通道开放剂Pinacidil(P + I / R)和干预组与KATP通道阻断剂5-HD(5-HD + P + I / R和5-HD + I / R)。通过常规全细胞膜片钳和多导管灌注系统技术测量每组的I_f密度,并绘制每组的I_f激活曲线。结果:①在不同方向电位下,与对照组相比,I / R组SAN细胞的I_f密度显着增加(P <0.01); P + I / R组与I / R组相比有明显下降(P <0.01); 5-HD + P + I / R组和5-HD + I / R组的I_f密度值与P + I / R组相比显着增加,但与I / R组无明显差异。 ②与对照组比较,SAN细胞的I_f激活曲线在极限激活电位下向右移动,一半从-108.0±12.4到-89.5±7.2mV(P <0.01);与I / R组相比,SAN细胞的I_f激活曲线在极限激活电位下向左移动,其中一半为-99. 5 +-10. 8 mV(P <0.05); KATP通道阻断剂5-HD可以阻断Pinacdil对I_f激活曲线的影响。结论:KATP通道开放剂吡那地尔可以拮抗模拟I / R对SAN细胞I_f的作用,这可能有利于维持模拟I / R条件下离子稳态的相对稳定性和电生理活性。

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