We studied the electrical properties of intact muscle fibers from normal and malignant hyperthermia-susceptible (MHS) pigs. Resting membrane potentials, action potentials, and current-voltage relationships were measured with and without the presence of halothane. There were no changes in the resting
Effects of hyperthermia on the membrane potential and Na+ transport of V79 fibroblasts
✍ Scribed by Ross B. Mikkelsen; Craig R. Asher
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 629 KB
- Volume
- 144
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
The effects of hyperthermia (41–43°C) on the membrane potential (calculated from the transmembrane distribution of [^3^H]tetraphenylphosphonium) and Na^+^ transport of Chinese hamster V79 fibroblasts were studied. At 41°C, hyperthermia induced a membrane hyperpolarization of log phase cells (5 to 26 mV) that was reversible upon returning to 37°C. The hyperpolarization was inhibited 50% by 1 mM ouabain or 0.25 mM amiloride, an inhibitor of Na^+^: H^+^ exchange. Shifting temperature to 41°C increased ouabain‐sensitive Rb^+^ uptake indicating activation of the electrogenic Na^+^ pump. At 43°C for 60 min, the membrane potential of log phase cells depolarized (20–35 mV). Parallel studies demonstrated enhanced Na^+^ uptake at 41°C only in the presence of ouabain. At 43°C, Na^+^ uptake was increased relative to controls with or without ouabain present. At both 41 and 43°C, 0.25 mM amiloride inhibited heat‐stimulated Na^+^ uptake. Na^+^ efflux was enhanced at 41°C in a process inhibited by ouabain. Thus, one consequence of heat treatment at 41°C is activation of Na^+^:H^+^ exchange with the resultant increase in cytosolic [Na^+^] activating the electrogenic Na^+^ pump. At temperatures ≥43°C, the Na^+^ pump is inhibited.
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