萎缩比目鱼肌钾离子通道改变对高频强直收缩疲劳性的作用

Effects of K^+ Channel Alteration on Fatigability of High-frequency Tetanic Contraction in Mouse Atrophic Soleus.

目的探讨萎缩比目鱼肌高频强直收缩疲劳性增加涉及细胞膜离子通道的可能机理。方法建立小鼠尾部悬吊模型模拟失重状态,用离体骨骼肌肌条灌流方法,分别观测在10mmol/L钾离子和60mmol/L钠离子灌流液灌流下,小鼠比目鱼肌高频强直收缩功能的变化。结果在生理溶液灌流下,悬吊1周组小鼠比目鱼肌高频强直收缩的最大张力(Po)与其同步对照组相比,仅有降低趋势;但是,高频强直收缩第33秒收缩张力与最大张力之比(P33/Po)却明显降低。尾部悬吊1周组小鼠比目鱼肌高频强直收缩后恢复时间短于正常对照组。与生理溶液灌流相比,高钾灌流的悬吊1周组与对照组比目鱼肌的Po均明显降低,两组P33/Po也显著降低,即疲劳性增加;低钠灌流的对照组比目鱼肌的P33/Po呈显著性降低,但悬吊组增高。在高钾灌流条件下,对照组比目鱼肌等长收缩的阈刺激电压无明显改变,而悬吊1周组则明显降低;在低钠灌流条件下,对照组和悬吊1周组比目鱼肌等长收缩阈刺激电压均显著增高。结论萎缩比目鱼肌纤维膜上K+通道的改变,可能是引起其高频强直收缩疲劳性增加的主要因素。

Objective To elucidate the underlying mechanisms of the high fatigability in mouse atrophic soleus during high-frequency tetanic contraction. Method A tail-suspended mouse model was employed to simulate weightlessness on the ground. Soleus muscle strips were perfused in vitro with Krebs-Henseleit solution containing 10 mmol/L K^＋ （HK） or 60 mmol/L Na^＋ （LNa）. The contractile function of muscle strips was observed during high-frequency stimulation. Result Maximal tension （P0） of soleus tetanic contraction showed no difference between control （CON） and 1-week tail-suspension group（SUS）. P33/P0（ P33, transient tension of tetanic contraction at the 33 s） was reduced significantly in SUS, and it manifested an increase in fatigability during tetanic contraction in SUS. After high-frequency tetanic contraction, the recover time of isometric tension was shortened in SUS. Comparing with Krebs-Henseleit solution perfusion, Po and P33/P0 of soleus were lower under HK perfusion, but no difference in Po between CON and SUS; however, P33/P0 decreased more in SUS than in CON. LNa perfusion induced an increase in P33/P0 of SUS, but decrease in that of CON. The threshold stimulating voltage was decreased in SUS soleus which were perfused with HK, but no change in CON. The threshold stimulating voltage showed an increase in both CON and SUS under LNa perfusion. Conclusion These results suggest that the changes in K^＋ channel characteristics may increase the fatigability during high-frequency tetanic contraction in atrophic soleus.