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目的 :探讨迷走神经递质乙酰胆碱 (ACh)对家兔窦房结细胞动作电位、毒蕈碱型钾离子流 (IK,ACh)、钙离子流(ICa)及超极化激活的离子流 (If)的影响及脱敏可能的离子机制。方法 :采用全细胞膜片钳技术分别记录了单个家兔窦房结细胞的各种通道离子流及动作电位。结果 :1当给单个心脏窦房结细胞灌注 ACh时 ,可使其自发电活动减慢 ,甚至消失。而当持续灌注 ACh时 ,可出现其负性变率作用的脱敏现象 ,即尽管 ACh持续存在 ,窦房结细胞的自发电活动逐渐恢复。 2 ACh可以激活 IK,ACh,IK,ACh随着 ACh的持续灌注可出现脱敏现象。 3ACh对“基础”钙离子流 (ICa)无明显作用 ,但当钙离子流被 β受体激动剂异丙肾上腺素增大之后 ,ACh可以降低此钙通道离子流。ACh的作用并未出现脱敏现象。 4ACh可以降低单个窦房结细胞的超极化激活的离子流 (If)。这个效应也没有脱敏的现象。结论 :ACh对心脏所致的负性变率作用的脱敏现象主要是毒蕈碱型钾通道 IK,ACh脱敏的缘故。
Objective: To investigate the effect of vagal neurotransmitter acetylcholine (ACh) on the action potentials, muscarinic potassium currents (IK, ACh), calcium currents (ICa) and hyperpolarization ion currents (If) And the possible ion mechanism of desensitization. Methods: The whole-cell patch clamp technique was used to record the ion channel currents and action potentials of various channels of single rabbit sinoatrial node cells. Results: 1 When a single heart sinoatrial cells perfusion ACh, can slow down its self-generating activity, or even disappear. When ACh was continuously perfused, the desensitization phenomenon of negative variability could occur. That is, although ACh persisted, the self-generating activity of sinoatrial node cells gradually recovered. 2 ACh can activate IK, ACh, IK, ACh desensitization with continuous perfusion of ACh. 3ACh had no significant effect on the “basal” calcium flux (ICa), but ACh decreased this calcium channel flux when the calcium flux was increased by the isoprenaline, a beta-agonist. The role of ACh did not appear desensitization. 4ACh reduces hyperpolarization-activated ion currents (If) in a single sinoatrial node cell. This effect is also no desensitization phenomenon. CONCLUSION: The desensitization of ACh to cardiac-induced negative rate of change is mainly due to the desensitization of IK and ACh in muscarinic potassium channel.