Gutierrez G, Kiiski R, Fernandez E, Lee D H
Department of Internal Medicine, University of Texas Houston Health Science Center 77030, USA.
J Crit Care. 1996 Dec;11(4):197-205. doi: 10.1016/s0883-9441(96)90031-3.
Skeletal muscle fatigue has been associated with potassium efflux from the myocytes, resulting in endogenous increases in blood potassium concentration ([K+]). Conversely, exogenous increases in extracellular [K+] potentiates contraction in isolated muscle preparations. The mechanisms responsible for these contradictory effects of [K+] on skeletal muscle function are unknown. Moreover, little is known about the effect of exogenous increases in [K+] on force generation by intact animals, given potassium's deleterious effect on cardiac function.
We compared the response to exogenous increases in blood [K+] in rabbits given an infusion of potassium chloride (KCl) intravenously (IV) (0.2 mol/L; KCl group; n = 7) to a group given 0.9% sodium chloride (NaCl) (control; n = 7). The rabbits underwent low-frequency, isometric twitch stimulation of the left hindlimb (square wave pulses 100 microseconds, 40V, 0.25 Hz) throughout the experiment. Both groups received 0.9% NaCl (25 mL/h) during the first hour of twitch stimulation and experienced similar decreases in hindlimb forces to 70% of initial force. A continuous infusion of KCl or of saline (60 mL/h) was started, and hindlimb stimulation continued for 2 hours.
There were no changes in [K+] in the control group, and twitch forces progressively declined during the next 2 hours (369 +/- 47 g to 279 +/- 34 g, P < .01). Arterial [K+] increased in the KCl group from 2.6 +/- 0.1 to 10.1 +/- 0.5 mmol/L (P < .01), and hindlimb twitch forces almost doubled (418 +/- 49 g to 756 +/- 55 g, P < .01). Force frequency curves showed improved contractility in the KCl group at stimulation frequencies below 30 Hz.
Exogenous increases in blood [K+] potentiate skeletal muscle contraction in intact animals and reverse low-frequency twitch fatigue. A possible mechanism may be the maintenance of intracellular [K+] by hindering K+ efflux from skeletal muscle cells.
骨骼肌疲劳与钾从肌细胞外流有关，导致血钾浓度（[K+]）内源性升高。相反，细胞外[K+]的外源性升高会增强离体肌肉标本的收缩。[K+]对骨骼肌功能产生这些矛盾作用的机制尚不清楚。此外，鉴于钾对心脏功能的有害影响，关于外源性[K+]升高对完整动物力量产生的影响知之甚少。
我们比较了静脉输注氯化钾（KCl）（0.2 mol/L；KCl组；n = 7）的兔子与输注0.9%氯化钠（NaCl）的兔子（对照组；n = 7）对外源性血钾升高的反应。在整个实验过程中，对兔子的左后肢进行低频等长抽搐刺激（方波脉冲100微秒，40V，0.25 Hz）。两组在抽搐刺激的第一个小时内均接受0.9% NaCl（25 mL/h），后肢力量均出现类似下降，降至初始力量的70%。开始持续输注KCl或生理盐水（60 mL/h），后肢刺激持续2小时。
对照组[K+]无变化，在接下来的2小时内抽搐力量逐渐下降（369±47 g至279±34 g，P <.01）。KCl组动脉血[K+]从2.6±0.1 mmol/L增加到10.1±0.5 mmol/L（P <.01），后肢抽搐力量几乎翻倍（418±49 g至756±55 g，P <.01）。力量频率曲线显示，在刺激频率低于30 Hz时，KCl组的收缩能力有所改善。
外源性血钾升高可增强完整动物的骨骼肌收缩，并逆转低频抽搐疲劳。一种可能的机制可能是通过阻止钾从骨骼肌细胞外流来维持细胞内[K+]。
