Ellingsen O, Vengen O A, Sejersted O M, Ilebekk A
Institute for Experimental Medical Research, University of Oslo, Norway.
Acta Physiol Scand. 1988 Feb;132(2):241-50. doi: 10.1111/j.1748-1716.1988.tb08323.x.
Lower intracellular Na+ during beta-adrenergic stimulation provides an increased driving force for Na-Ca exchange, which might attenuate the inotropic response. Since (1) Na+ reduction is coupled to K+ uptake, and (2) K+ uptake lags behind the positive inotropic response to isoproterenol, we could examine the effect of Na-Ca exchange by comparing cardiac contractility and K+ balance following intracoronary isoproterenol infusion (0.6-0.8 microgram min-1). In 8 open-chest pigs, potassium concentrations were continuously measured by PVC-valinomycin mini-electrodes in arterial blood (a), and in myocardial venous blood in a shunt from the coronary sinus (cs) to the right atrium. Shunt flow, aortic flow, a left ventricular segment length and left ventricular pressure (LVP) were also continuously recorded. 64 (41-85)% (median and 95% confidence interval) of the LV dP/dt increase occurred within 1 min; thereafter contractility rose slowly. During the first minute of isoproterenol infusion, there was a small net myocardial K+ release, which then reversed to K+ accumulation. A maximum a-cs K+ concentration difference of 0.20 (0.09-0.39) mM occurred at 3.0 (2.0-4.25) min, falling to 0.05 (0.01-0.10) mM after 6.5 (3.75-8.75) min, at which point accumulated myocardial K+ uptake was 135 (27-219) mumol 100 g-1. Heart rate remained unchanged and intramural ECG indicated no sign of ischemia during the first 1.5 min of isoproterenol infusion. At 6.25 (5.0-8.0) min after stop of isoproterenol, LV dP/dt was 12 (9-24)% lower than before infusion (P less than 0.02) whereas myocardial K+ content remained higher than control. Thus, the monovalent cation shift succeeding the positive inotropic response was not associated with reduced contractility, but could explain the undershoot of LV dP/dt after stopping isoproterenol.
β-肾上腺素能刺激期间细胞内钠离子浓度降低，会增加钠-钙交换的驱动力，这可能会减弱心肌收缩反应。由于（1）钠离子减少与钾离子摄取相关，且（2）钾离子摄取滞后于异丙肾上腺素的正性肌力反应，因此我们可以通过比较冠状动脉内输注异丙肾上腺素（0.6 - 0.8微克·分钟⁻¹）后心脏收缩力和钾离子平衡来研究钠-钙交换的作用。在8只开胸猪中，通过聚氯乙烯-缬氨霉素微型电极连续测量动脉血（a）以及从冠状窦（cs）到右心房的分流中的心静脉血中的钾离子浓度。还连续记录分流流量、主动脉流量、左心室节段长度和左心室压力（LVP）。左心室dP/dt增加的64（41 - 85）%（中位数和95%置信区间）在1分钟内出现；此后收缩力缓慢上升。在输注异丙肾上腺素的第一分钟内，有少量心肌净钾离子释放，随后转变为钾离子蓄积。在3.0（2.0 - 4.25）分钟时，动脉血与心静脉血之间的最大钾离子浓度差为0.20（0.09 - 0.39）毫摩尔，在6.5（3.75 - 8.75）分钟后降至0.05（0.01 - 0.10）毫摩尔，此时心肌钾离子蓄积摄取量为135（27 - 219）微摩尔·100克⁻¹。在输注异丙肾上腺素的前1.5分钟内，心率保持不变，壁内心电图未显示缺血迹象。在停止输注异丙肾上腺素后6.25（5.0 - 8.0）分钟时，左心室dP/dt比输注前低12（9 - 24）%（P < 0.02），而心肌钾离子含量仍高于对照组。因此，正性肌力反应后单价阳离子的转移与收缩力降低无关，但可以解释停止输注异丙肾上腺素后左心室dP/dt的回落。
