Ellingsen O, Vengen O A, Kjeldsen S E, Eide I, Ilebekk A
Institute for Experimental Research, University of Oslo, Norway.
Cardiovasc Res. 1987 Dec;21(12):892-901. doi: 10.1093/cvr/21.12.892.
To determine whether sympathetic nerve stimulation induces a significant potassium uptake in the myocardium, the changes in myocardial potassium balance, catecholamine release, lactate uptake, and oxygen consumption were recorded in eight anaesthetised open chest pigs during electrical stimulation of the right intermediate cardiac nerve at 10 Hz. Potassium concentrations were continuously measured by polyvinylchloride valinomycin minielectrodes in arterial and coronary sinus blood. Potassium concentration in coronary sinus blood fell to a nadir 0.42(0.21-0.61) mmol.litre-1 below control values (median and 95% confidence interval) and resulted in a peak potassium uptake of 65(38-102) mumol.min-1 100 g-1 after 2.5(2.0-3.0) min, which correlated (r = 0.94, p less than 0.001) with cardiac noradrenaline release. Accumulated myocardial potassium uptake amounted to 139(82-241) mumol.100 g-1 when a stable potassium concentration difference between arterial and coronary sinus blood was reached after 5.5(4.25-6.50) min. Cardiac contractility (LV dP/dt), myocardial oxygen consumption, and lactate uptake rose from control to peak potassium uptake (p less than 0.001) by 140%, 158%, and 92% respectively. Coronary sinus blood noradrenaline and adrenaline concentrations rose significantly (p less than 0.01) from 58(44-87) pg.ml-1 at control to 2208(1159-5627) pg.ml-1 at peak uptake and from 15(11-19) pg.ml-1 to 85(64-230) pg.ml-1 respectively. Arterial noradrenaline increased from 29(19-41) pg.ml-1 to 374(176-640) pg.ml-1 and arterial adrenaline rose from 15(11-23) pg.ml-1 to 31(24-52) pg.ml-1 (p less than 0.001). It is concluded that sympathetic nerve stimulation induces a substantial myocardial potassium uptake in a dose dependent relation to cardiac noradrenaline release and alters the contractile and metabolic state of the heart substantially with only minor changes in arterial catecholamine concentration.
为了确定交感神经刺激是否会在心肌中引起显著的钾摄取，在8只麻醉开胸猪中，以10赫兹的频率电刺激右侧中间心神经时，记录了心肌钾平衡、儿茶酚胺释放、乳酸摄取和氧消耗的变化。通过聚氯乙烯缬氨霉素微电极连续测量动脉血和冠状窦血中的钾浓度。冠状窦血中的钾浓度降至比对照值低0.42（0.21 - 0.61）毫摩尔·升⁻¹的最低点，并在2.5（2.0 - 3.0）分钟后导致峰值钾摄取量为65（38 - 102）微摩尔·分钟⁻¹·100克⁻¹，这与心脏去甲肾上腺素释放相关（r = 0.94，p < 0.001）。当在5.5（4.25 - 6.50）分钟后动脉血和冠状窦血之间达到稳定的钾浓度差时，累积的心肌钾摄取量达到139（82 - 241）微摩尔·100克⁻¹。心脏收缩力（左心室dp/dt）、心肌氧消耗和乳酸摄取从对照值上升到峰值钾摄取时（p < 0.001），分别增加了140%、158%和92%。冠状窦血中的去甲肾上腺素和肾上腺素浓度显著升高（p < 0.01），从对照时的58（44 - 87）皮克·毫升⁻¹分别升至峰值摄取时的2208（1159 - 5627）皮克·毫升⁻¹和从15（11 - 19）皮克·毫升⁻¹升至85（64 - 230）皮克·毫升⁻¹。动脉血中的去甲肾上腺素从29（19 - 41）皮克·毫升⁻¹增加到374（176 - 640）皮克·毫升⁻¹，动脉血中的肾上腺素从15（11 - 23）皮克·毫升⁻¹升至31（24 - 52）皮克·毫升⁻¹（p < 0.001）。结论是，交感神经刺激以与心脏去甲肾上腺素释放呈剂量依赖性的关系诱导心肌大量摄取钾，并显著改变心脏的收缩和代谢状态，而动脉血中儿茶酚胺浓度仅有微小变化。
