首页 | 本学科首页   官方微博 | 高级检索  
     

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
引用本文:冯汉忠,余志斌. 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[J]. 航天医学与医学工程, 2005, 18(5): 329-333
作者姓名:冯汉忠  余志斌
作者单位:第四军医大学航空航天生理学教研室,陕西,西安,710032;第四军医大学航空航天生理学教研室,陕西,西安,710032
基金项目:第四军医大学创新工程(CX02A005)与骨干人才(2004年度)资助
摘    要: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(P0)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/P0)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P0均明显降低,两组P33/P0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/P0也显著性降低,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。

关 键 词:失重模拟  尾吊  比目鱼肌  疲劳性  K+通道
文章编号:1002-0837(2005)05-0329-05
收稿时间:2005-01-15
修稿时间:2005-01-15

Effects of K+ Channel Alteration on Fatigability of High-frequency Tetanic Contraction in Mouse Atrophic Soleus
FENG Han-zhong,YU Zhi-bin. Effects of K+ Channel Alteration on Fatigability of High-frequency Tetanic Contraction in Mouse Atrophic Soleus[J]. Space Medicine & Medical Engineering, 2005, 18(5): 329-333
Authors:FENG Han-zhong  YU Zhi-bin
Abstract: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(P_o) of soleus tetanic contraction showed no difference between control(CON) and 1-week tail-suspension group(SUS). P_ 33 /P_o(P_ 33 , 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, P_o and P_ 33 /P_o of soleus were lower under HK perfusion, but no difference in P_o between CON and SUS; however, P_ 33 /P_o decreased more in SUS than in CON. LNa perfusion induced an increase in P_ 33 /P_o 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.
Keywords:weightlessness simulation  tail suspension  soleus muscle  fatigability  K~ channel
本文献已被 CNKI 维普 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号