Fong C N, Atwood H L, Charlton M P
Exp Neurol. 1986 Aug;93(2):359-68. doi: 10.1016/0014-4886(86)90196-2.
Intrafiber Na+-activity, (aNa)i, was measured in vivo in single muscle fibers in the gastrocnemius and soleus muscles of normal and dystrophic (dy2J/dy2J) C57BL/6J mice by means of double-barrel Na+-selective microelectrodes. Values of (aNa)i in normal gastrocnemius and soleus muscles were 9.8 +/- 1.0 mM (means +/- SE; N = 15) and 13.7 +/- 1 mM (N = 19), respectively. Values of (aNa)i in dystrophic gastrocnemius and soleus muscles were 18.7 +/- 1.3 mM (N = 10) and 26.2 +/- 3.3 mM (N = 15), respectively. The soleus muscle of both normal and dystrophic mice was "Na+ loaded" by an intermittent tetanus delivered via the sciatic nerve. Muscles from both normal and dystrophic mice could extrude the Na+ load at similar rates. The results suggest that in the dystrophic mice the elevated (aNa)i is not due to inability of the Na+ pump to respond to a Na+ load; rather, it may be due to an alteration in the affinity of the pump for Na+, resulting in a different "set point" for (aNa)i.
通过双管钠选择性微电极，在正常和营养不良（dy2J/dy2J）的C57BL/6J小鼠的腓肠肌和比目鱼肌的单根肌纤维中，对纤维内钠活性（aNa）i进行了体内测量。正常腓肠肌和比目鱼肌的（aNa）i值分别为9.8±1.0 mM（平均值±标准误；N = 15）和13.7±1 mM（N = 19）。营养不良的腓肠肌和比目鱼肌的（aNa）i值分别为18.7±1.3 mM（N = 10）和26.2±3.3 mM（N = 15）。通过坐骨神经传递的间歇性强直刺激，使正常和营养不良小鼠的比目鱼肌都“钠负荷”。正常和营养不良小鼠的肌肉都能以相似的速率排出钠负荷。结果表明，在营养不良小鼠中，升高的（aNa）i并非由于钠泵无法对钠负荷做出反应；相反，可能是由于泵对钠的亲和力发生改变，导致（aNa）i有不同的“设定点”。
