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作 者:刘华军[1,2] 陈灏珠[1,2] 杨学义[1,2] 程介士
机构地区:[1]上海医科大学中山医院上海市心血管病研究所 [2]上海医科大学医学神经生物学国家重点实验室
出 处:《中华心血管病杂志》1997年第2期85-88,共4页Chinese Journal of Cardiology
摘 要:目的:建立豚鼠心肌细胞低氧复氧模型,研究低氧复氧对心肌细胞ATP敏感性钾通道及L型钙通道电流(ICa-L)的影响,以探讨心肌低氧时动作电位时程(APD)缩短的机制。方法:采用膜片钳技术记录豚鼠心肌细胞动作电位、钾通道电流及钙通道电流。结果:发现低氧5~20分钟后豚鼠心肌细胞APD明显缩短(由384±65ms降至188±46ms,P<0.05),外向性钾电流明显增加,电流-电压曲线随去极化增加呈线性变化,且能被优降糖所抑制,显示ATP敏感性钾通道开放。低氧可抑制ICa-L,ICa-L峰值降低(由1.35±0.18nA降至0.76±0.21nA,P<0.05),电流-电压曲线上移,复氧后APD可很快恢复,ICa-L则不能恢复。结论:本研究提示低氧时豚鼠心肌细胞APD缩短不仅为ATP敏感性钾通道开放所致,而且尚有内向性钙电流抑制过程参与。The objectives of this study were (1) to develop a cellular model of hypoxia and reoxygenation in isolated cardiomyocytes, (2) to determine the ionic channel basis of action potential during hypoxia and reoxygenation. Cardiomyocytes were isolated from adult guinea pig ventricles and the patch clamp technique in the whole cell configuration was used to study ionic current. The experiments were performed in a special chamber that allowed the cells to be exposed to a sufficiently low oxygen pressure. The results showed that action potential duration (APD) abbreviated after 5 to 20 minutes' hypoxia (384±65 ms vs 188±46 ms, P <0.05). The time independent outward currents, which had a linear current voltage relation between 100 mv and+100 mv, increased significantly and could be blocked by 5 10 μmol/L glibenclamide and inhibited by the diffusion of 3 mmol/L ATP into the pipette. At the same time, I Ca L decreased nearly 50%. Upon reoxygenation, APD recovered gradually while I Ca L did not. It is concluded that the hypoxia induced outward current is related to not only the opening of ATP sensitive potassium channels but also the inhibition of inward calcium current.
分 类 号:R542.202[医药卫生—心血管疾病]
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