Sympathetic innervation in rat cultured cardiac myocytes increases the effect of ischemic precondtioning

为探讨交感神经支配是否对心肌缺血引起的心肌损伤具有保护作用，我们在体外培养的大鼠心肌细胞上，分别观察了肌膜<ATP>钾通道开放剂吡那地尔、代谢抑制剂氰化物和线粒体钾通道开放剂二氮嗪对心肌细胞膜和线粒体钾通道<ATP>电流的影响;用1日龄未受交感神经支配的新生大鼠心肌细胞、与交感神经节共培养的心肌细胞和去交感神经支配的心肌细胞培养心肌细胞。吡<ATP>那地尔使交感神经支配的心肌细胞钾通道外向电流（56.8±5.2^*）明显增加，与去交感神经支配的心肌细胞（10.8±3.4）和去交感神经支配的心肌细胞（9.8±3.1）相比有显著性差异（p&lt;0.05）。氰化物和重氮盐的应用得到了几乎相同的结果。结果表明，交感神经支配使心肌细胞膜和线粒体钾<ATP>通道电流增加。钾电流增加<ATP>可缩短心室肌动作电位时程，对缺血心肌细胞钙超载有保护作用。因此，交感神经支配可以通过激活肌膜和线粒体K_通道来保护缺血心肌的心肌扰动<ATP>。

To clarify whether sympathetic innervation protects myocardial disturbance caused by myocardial ischemeia in rat cardiac myocyte, we evaluated sarcolemmal or mitochondorial K_<ATP> channel currents induced by Pinacidil which is sarcolemmal channel opener, Cyanide which is metabolic inhibitor, and Diazoxide which is mitochondrial K_<ATP> channel opener in next cultured or co-cultured myocytes ; cultured myocytes using 1day old neonatal rat cardiac myocytes which was not sympathetic innervation until 1day old, co-cultured cardiac myocytes with sympathetic ganglion, and denervaed cardiac myocytes. Outward current of K_<ATP> channel was significantly increased after application of Pinacidil in sympathetic innervated myocytes (56.8±5.2^*) compared to those in myocytes (10.8±3.4) and denervated myocytes (9.8±3.1) (p<0.05). Almost same results were obtained by application of Cyanide and Diazoxide. These show that sarcolemmal and mitochondorial K_<ATP> channel currents were increased by sympatheic innervation. Increased K_<ATP> current leads shortening of ventricular myocardial action potential duration and may protect Ca^<2+> overloading in ischemic ventricular myocytes. Thus, sympathetic innervation could be protected myocardial disturbance in ischemic myocardium by activation of sarcolemmal and mitochondrial K_<ATP> channels.