Heparin Mediates Transmembrane Potassium Transfer in Hyperkalemic Dogs

Abstract

Abstract

Unheparinized, ureter-ligated control dogs that are potassium loaded, i.e., infused with 2 mEq of KCl/kg until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear (end point), transfer 57 ± 4% (1.7 ± 0.1 mEq/kg) of administered potassium to intracellular fluid. Heparinized controls transfer 73 ± 1% (3.2 ± 0.2 mEq/kg); with simultaneous α-adrenoreceptor blockade, that proportion increases to 81 ± 2% (4.80 ± 0.7 mEq/kg) and with simultaneous β-receptor blockade it is 58 ± 3% (1.1 ± 0.1 mEq/kg). In potassium loaded, ureter-ligated dogs, heparin increases transmembrane potassium transfer as effectively as does a dosage of atropine large enough to cross the blood-brain barrier and its influence on potassium transfer, like that of atropine, is suppressed by β-adrenoreceptor blockade.