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对代谢耗竭肌纤维中膜常数和钾电导的评估。

An evaluation of the membrane constants and the potassium conductance in metabolically exhausted muscle fibres.

作者信息

Fink R, Lüttgau H C

出版信息

J Physiol. 1976 Dec;263(2):215-38. doi: 10.1113/jphysiol.1976.sp011629.

DOI:10.1113/jphysiol.1976.sp011629
PMID:1087932
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1307698/
Abstract
  1. The membrane characteristics of metabolically poisoned and mechanically exhausted frog skeletal muscle fibres were investigated with intracellular micro-electrodes. 2. When cyanide plus iodoacetate were applied as metabolic poisons twitch tension declined towards zero after 150-300 stimuli (0-3 Hz; temperature = 0 degrees C). At the beginning of stimulation the mean resting potenial fell from -75 to -69 mV; it rose subsequently to -83 mV. The membrane resistance decreased during this stimulation period along a sigmoid time course to 4-6% of the original value. 3. In completely exhausted fibres the following membrane constants were estimated (23 degrees C): length constant, 0-31 mm; input resistance, 31 komega; membrane resistance, 58 omega.cm2. These values were calculated under the assumption of a constant internal resistivity of 170 omega. cm. The Q10 values of these constants were similar to those in normal fibres. Afew experiments revealed that the membrane capacity remained roughly constant under these conditions. 4. The current-voltage relation of exhausted fibres was approximately linear in the range between -60 and -100 mV. At less negative potentials the conductance increased slightly while at more negative potentials it decreased. The latter, in particular, became more evident when the imput current was converted into membrane current density by applying Cole's theorem. 5TEA+ and Rb+ in the external solution increased the membrane resistance of exhausted fibres by more than one order of magnitude. The major part of the membrane conductance induced by exhaustion, however, could not be blocked by these ions or Zn2+. 6. Chloride-free test solutions were used to measure the relative contributions of potassium and chloride ions to the membrane conductance. The relation GK:GC1 changed from 2:3 in normal fibres to 5:1 in exhausted ones. In absolute terms GK rose from ca. 130 to 14,300 mumho/cm2 and GC1 from ca. 200 to 2900 mumho/cm2. The discrimination between K+ and Na+ by the resting membrane in exhausted fibres was probably equal to or even higher than that under normal conditions. 7. In normal fibres the input resistance decreased by up to 20% after the external application of 1-2 mM caffeine, which is known to release calcium ions from internal stores. The elevation in internal Ca2+ by direct injection caused a small and, as a rule, irreversible decrease in input resistance which was probably partly due to local damage to the surface membrane. 8. It is concluded that in metabolically exhausted muscle fibres the surface and tubular membranes are still intact and that the observed decrease in membrane resistance is mainly due to an increase in potassium conductance. In addition, the results indicate that the gating mechanism of the potassium channels (presumably those with the characteristics of the slow component) is affected when energy reserves diminish.
摘要
  1. 用细胞内微电极研究了代谢中毒和机械疲劳的青蛙骨骼肌纤维的膜特性。2. 当使用氰化物加碘乙酸盐作为代谢毒物时,在150 - 300次刺激(0 - 3Hz;温度 = 0摄氏度)后,抽搐张力降至零。刺激开始时,平均静息电位从 - 75mV降至 - 69mV;随后又升至 - 83mV。在此刺激期间,膜电阻沿S形时间进程下降至原始值的4 - 6%。3. 在完全疲劳的纤维中,估计了以下膜常数(23摄氏度):长度常数,0 - 31mm;输入电阻,31kΩ;膜电阻,58Ω·cm²。这些值是在假设内部电阻率为170Ω·cm恒定的情况下计算得出的。这些常数的Q10值与正常纤维中的相似。一些实验表明,在这些条件下膜电容大致保持恒定。4. 疲劳纤维的电流 - 电压关系在 - 60至 - 100mV范围内近似线性。在负电位较小的情况下,电导略有增加,而在负电位较大时则减小。当通过应用科尔定理将输入电流转换为膜电流密度时,后者尤其明显。5. 外部溶液中的TEA⁺和Rb⁺使疲劳纤维的膜电阻增加了一个多数量级以上。然而,疲劳引起的膜电导的主要部分不能被这些离子或Zn²⁺阻断。6. 无氯测试溶液用于测量钾离子和氯离子对膜电导的相对贡献。GK:GC1的关系从正常纤维中的2:3变为疲劳纤维中的5:1。绝对而言,GK从约130μmho/cm²升至14300μmho/cm²,GC1从约200μmho/cm²升至2900μmho/cm²。疲劳纤维中静息膜对K⁺和Na⁺的区分可能等于甚至高于正常条件下的区分。7. 在正常纤维中,外部施加1 - 2mM咖啡因后,输入电阻降低高达20%,已知咖啡因会从内部储存中释放钙离子。通过直接注射使内部Ca²⁺升高会导致输入电阻出现小的且通常不可逆的降低,这可能部分是由于表面膜的局部损伤。8. 得出的结论是,在代谢疲劳的肌肉纤维中,表面膜和管状膜仍然完整,观察到的膜电阻降低主要是由于钾电导增加。此外,结果表明,当能量储备减少时,钾通道的门控机制(可能是那些具有慢成分特征的通道)会受到影响。

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