Rewarming of cold-incubated cat papillary muscles suggests activation of a ouabain-sensitive electrogenic mechanism for active Na extrusion, followed by passive K uptake.
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No immediate clinical implications; leaves open translation of ouabain-sensitive ion recovery mechanisms to human myocardium.
The cells of cat right ventricular papillary muscles were depleted of K and caused to accumulate Na and water by preincubation at 2-3 degrees C. The time courses of changes in cellular ion content and volume and of the resting membrane potential (V(m)) were then followed after abrupt rewarming to 27-28 degrees C. At physiological external K concentration ([K](o) = 5.32 mM) recovery of cellular ion and water contents was complete within 30 minutes, the maximal observable rates of K uptake and Na extrusion (Deltammol cell ion/(kg dry weight) (min.)) being 3.4 and 3.6, respectively. The recovery rate was markedly slowed at [K](o) = 1.0 mM. Rewarming caused V(m) measured in cells at the muscle surface to recover within from <1 to 9 minutes, but only slight restoration of cellular ion contents (measured in whole muscles) had occurred after 10 minutes. Studies of recovery in NaCl-free sucrose Ringer's solution made it possible to separate the ouabain-insensitive outward diffusion of Na as a salt from a simultaneous ouabain-sensitive Na extrusion which is associated with a net cellular K uptake. A hypothesis consistent with these observations is that rewarming may activate a ouabain-sensitive "electrogenic" mechanism, most probably the net active transport of Na out of the cell, from which net K uptake may then follow passively.
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Page et al. (1965) studied this question.
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