Abstract
Study in normal subjects of potassium movement and associated changes in skeletal muscle function yielded the following results: 1. 1. Muscle contraction caused movement of potassium out of muscle, as indicated by change in the arteriovenous difference in the exercised extremity. There was some evidence to suggest that rest had the opposite effect. 2. 2. During hypopotassemia following administration of glucose, and possibly following epinephrine, there was evidence of movement of potassium into muscle, while following insulin there was evidence of movement of the ion out of muscle and into some other site, presumably the liver. 3. 3. Hyperpotassemia produced by administration of potassium chloride was accompanied by movement of potassium into muscle. Muscle contraction then caused greater loss of potassium from the exercised extremity. 4. 4. Following tetanic muscle contraction or the administration of potassium chloride, and concomitant with a probable decrease in the ratio of intracellular to extracellular concentration of potassium, there was an increase in muscle contractility and in the ease of depolarization by ACh or neostigmine. These changes are attributed to a reduction in the resting muscle membrane potential resulting from the decrease in concentration ratio. 5. 5. Following the administration of insulin and glucose, and concomitant with a presumed increase in the concentration ratio of potassium, there was a slight decrease in the ease of depolarization by ACh. This change is attributed to an increase in the resting muscle membrane potential resulting from the increased concentration ratio. 6. 6. It is suggested that severe weakness may be infrequent in hyperkalemia, and in hypokalemia due to deficient intake or excessive loss of potassium or the administration of insulin and glucose, because the intracellular concentration of potassium may change in the same direction as the extracellular concentration in each instance, tending to limit the change in concentration ratio.
Published Version
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