【摘要】 神经递质乙酰胆碱 (ACh)调节心脏功能最重要的离子通道就是毒蕈碱型钾通道 (iK ,ACh) ,该通道由ACh经鸟苷酸调节蛋白 (G蛋白 )的 βγ亚单位而激活。本实验采用全细胞膜片箝方法 ,观察了麻醉药氟烷对豚鼠心房肌细胞iK ,ACh的影响。氟烷对iK ,ACh电流具抑制效应 ,灌注之后可使ACh激活的iK ,ACh速率减慢 ,峰值下降。但其抑制iK ,ACh的程度依激活方式而异 :经正常激活途径 ,即由ACh激活毒蕈碱M样受体的抑制程度比绕过受体直接激活G蛋白和钾通道时更为明显 ,表明氟烷对iK ,ACh的抑制作用 ,至少有一部分是对iK ,ACh通道及G蛋白的直接效应。氟烷可通过抑制iK ,ACh,从而影响副交感神经对心脏的支配作用更多还原

【Abstract】 Acetylcholine (ACh) released from parasympathetic nerves binds to muscarinic (M2) ACh receptor (mAChR) in the heart, which leads to activation of muscarinic K + channel via the βγ subunit of a G protein. The effect of a general anaesthetic (halothane) on the muscarinic K + channel (i K,ACh ) in guinea pig atrial cells was investigated using the whole cell patch clamp technique. Halothane supressed i K,ACh , slowed down activation of i K,ACh and decreased peak i K,ACh . When i K,ACh was activated by ACh acting via the muscarinic ACh receptors in the normal way, the decrease of i K,ACh was greater than the decrease when the muscarinic ACh receptor was bypassed and i K,ACh was activated by GTPγS. The above finding suggests that the suppression of i K,ACh by halothane is, in part, a result of the direct effect on the muscarinic K + channel or associated G protein. The decrease of i K,ACh by halothane may interfere with parasympathetic control of the heart.更多还原