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The movement of potassium ions in normal and dystrophic mouse muscle Burr, Lawrence Herbert


The radioactive isotope K⁴² was used to measure the rate of potassium exchange in muscle from 129 strain mice. The results followed an unique course if plotted as K⁴² uptake versus (external potassium concentration ∙ time) [superscript ½], and corresponded to the result predicted for K⁴² uptake mediated by an ion-exchange compartment in the muscle. Variations in external potassium concentration did not affect the uptake rate if plotted this way, but sodium ion exerted some effect on the rate. Dystrophic mouse tissue accumulated K⁴² more rapidly than did normal tissue, and the effect of varying the external potassium concentration did not alter this rate. The effects of sodium variation were more pronounced than in normal tissue. Inulin space of muscle was measured in vivo as well as in vitro, to enable a correction for K⁴² in the extracellular space to be made. The inulin space was found to decrease with increasing muscle size, and this was thought to be related to the development of the muscle. Dystrophic muscle exhibited more of a dependance of inulin space on muscle size than did normal muscle. The suggestion was made that the dystrophic muscle membrane might be abnormally permeable to inulin. Muscles were excised and assayed by flame photometry for sodium and potassium content. They were assayed when freshly excised, and also following incubation in a variant of Locke’s solution. The muscle cations were stable for the first two hours of incubation, but after this time, intracellular sodium rose and potassium fell. Fresh dystrophic mouse muscle had lower potassium and higher sodium content than normal fresh muscle. The cation changes following incubation resembled those found for normal muscle. The changes in intracellular cations were correlated with the K⁴² uptake results, and discussed in some detail.

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