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实验用胶原酶酶解法急性分离豚鼠心室肌细胞 ,利用全细胞膜片钳的方法记录心室肌细胞的延迟整流钾电流 (IK)、内向整流钾电流 (IK1)和ATP敏感钾电流 (IKATP)。采用低氧、无糖、高乳酸和酸中毒综合方式模拟缺血灌流 ,造成细胞的模拟缺血 ,并在缺血的基础上继续用含 10 0nmol/LAngⅡ灌流细胞 ,观察AngⅡ对模拟缺血心室肌细胞钾离子通道的影响。实验结果显示 :(1)模拟缺血时 ,IK 明显减小 ;AngⅡ能进一步抑制IK。 (2 )模拟缺血条件下 ,IK1受到抑制 ,并且以内向电流的抑制为主 ;AngⅡ可加强对IK1内向电流的抑制 ,而对部分外向电流则有增加的作用。 (3)模拟缺血使IKATP外向电流略有增加 ;AngⅡ则明显加强IKATP外向电流 ,此效应能被优降糖所阻断
The guinea pig ventricular myocytes were acutely isolated by collagenase digestion, and delayed rectifier potassium current (IK), inward rectifier potassium current (IK1) and ATP sensitive potassium current (IKATP) were recorded by whole cell patch clamp. Using hypoxia, sugar-free, lactic acid and acidosis comprehensive simulation of ischemic perfusion, resulting in simulated ischemia of the cells, and on the basis of ischemia continue to use 10 0nmol / LAng Ⅱ perfusion cells observed Ang Ⅱ on simulated ischemic ventricular Effect of K + channels in muscle cells. The experimental results showed that: (1) IK was significantly reduced in simulated ischemia; AngⅡ could further inhibit IK. (2) IK1 was inhibited under the condition of simulated ischemia, and the inhibition of inward current was the main one. AngⅡ enhanced the inhibition of IK1 inward current, but increased the part of outward current. (3) Simulated ischemia increased IKATP outward current slightly; while AngⅡ significantly increased IKATP outward current, which could be blocked by glyburide