Prolonged exposure to low-K Ringer solution potentiates contractility in bullfrog ventricle, likely mediated by Na-Ca exchange mechanisms.
Animal data on low-K effects should not alter clinical care; leaves open translation to mammalian myocardium.
1) The electrical and mechanical activity of bullfrog ventricle was investigated during and after a prolonged exposure to a K-depleted fluid, which was applied for the purpose of increasing the intracellular Na ions in exchange for K ions.2) There was a gradual increase in twitch tension during immersion in the K-depleted fluid in addition to the immediate potentiation by this solution. The action potential was slightly depressed in height during the immersion.3) There was also a relative reduction in the rate of relaxation of twitch with the gradual increase in tension, and the twitch pattern became a type of rapid onset and slow relaxation.4) The muscles treated with cold K-depleted fluid for an extremely long period of time (24 hr) showed a similar augmentation in contractility and a particularly high sensitivity to extracellular Na-depletion for generating a Na-lack contracture.5) Possible mechanisms relating the intracellular ionic environment to the myocardial contractility were discussed, and attempts were made to interprete the results in terms of Na-Ca exchange mechanism across the cell membrane or Na-Ca competition at the subcellular membrane sites.
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Tsuguhisa Ehara (1974) studied this question.
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