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Abstract
A marked increase in [Ca2+]i is provoked in isolated guinea-pig ventricular myocytes by return to normal Tyrode solution after a period of exposure to fluid free of divalent cations. When the sarcolemma of the myocyte remains intact, [Ca2+]i falls back towards initial levels over the next 5 to 10 min in spite of the strong irreversible contracture. This recovery fails to occur if either the Na+ pump or Na(+)-Ca2+ exchange is inhibited once [Ca2+]i has risen.
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