Key result
Calcium-tension relationships and maximal tensions of muscle fibers from patients with periodic paralysis were indistinguishable from those of normal subjects.
Observational (n=7)
Loss of calcium-induced myofibril contraction is not the cause of paralysis in periodic paralysis.
Does not implicate myofibrillar Ca sensitivity loss in periodic paralysis paralysis; reinforces need to target membrane excitability defects in future studies.
Lateral gastrocnemius muscle biopsies from a 26-year-old man with hyperkalemic periodic paralysis and a 23-year-old man with hypokalemic periodic paralysis were studied. Both patients came from families in which older relatives had developed a vacuolar myopathy in association with their periodic paralysis. Muscle fibers were chemically skinned, and individual fibers were studied with a low-compliance strain gauge. The tension generated by fibers was studied in baths with calcium concentrations from 10(-8) mol/L to 2.5 x 10(-5) mol/L. The Ca-tension relationships and maximal tensions (normalized to fiber cross-sectional area) of fast and slow twitch fibers were indistinguishable from those found in fibers from 5 normal subjects. The results reinforce earlier findings which suggested that loss of Ca-induced myofibril contraction was not the cause of paralysis in periodic paralysis.
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Robert L. Ruff (1991) conducted an observational in Periodic paralysis (n=7). Periodic paralysis vs. Normal subjects was evaluated on Ca-tension relationships and maximal tensions of fast and slow twitch fibers. Calcium-tension relationships and maximal tensions of muscle fibers from patients with periodic paralysis were indistinguishable from those of normal subjects.
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