麻醉剂氟烷对心脏毒蕈碱型钾通道的影响

神经递质乙酰胆碱（ＡＣｈ）调节心脏功能最重要的离子通道就暗毒蕈碱型钾通道（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。本实验彩全细胞膜片箝方法,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,峰植下降。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

Effect of halothane on the muscarinic potassium current of the heart

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 betagamma 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 suppressed 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 GTPgammaS. 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.