Dextrose-, adenosine- and magnesium-induced protective actions during anoxia and reperfusion in canine Purkinje tissue.

1. The effects of dextrose, magnesium (Mg) and adenosine on membrane potential and force of contraction were studied in driven and overdriven canine cardiac Purkinje tissue. 2. Dextrose (50 mmol/L) and adenosine (4-6 mmol/L) both showed protective action (the latter to a lesser extent) against simulated anoxia and reperfusion-induced arrhythmias, increased force of contraction transiently on reperfusion, and the former sustained the increase in force to a lower level as long as it was in the superfusing solution. 3. Dextrose (50 mmol/L) and Mg (5 mmol/L) restored overdrive-induced hyperpolarization during simulated anoxia. Adenosine was largely ineffective. 4. It was concluded that dextrose and adenosine (to a lesser extent) protect against arrhythmias by replenishing the critical intracellular pool of ATP which controls membrane transport of electrolytes such as K and Ca. Restoration of Na-K ATPase activity alone (as in the case of high Mg concentrations) is not sufficient to prevent arrhythmias.