Mechanism of myocardial injury in dogs with hypokalaemia.

Hypokalaemia was induced by infusing polystyrene sulphonate into the colon of mongrel dogs. Sixty minutes after infusion adrenaline 10 micrograms.kg-1 was injected intravenously, which had no effect on serum creatine kinase activity or myocardial histology in the control dogs. However, in dogs with hypokalaemia creatine kinase activity was increased, and pronounced histological changes were seen 60 min after injection. A clear reciprocal relation was found between serum potassium concentration and creatine kinase activity. Premedication with an alpha 1 blocking agent prevented the changes associated with hypokalaemia. Heart mitochondria were prepared from other dogs with hypokalaemia 5 min after adrenaline injection and their calcium content measured. Heart mitochondrial calcium content was increased in parallel with the decrease in serum potassium concentration. Alpha 1 blockade also prevented the increase in mitochondrial calcium content. These results indicate that the intracellular calcium concentration is considerably increased by alpha 1 receptor stimulus under hypokalaemic conditions and that this increase in calcium concentration plays a crucial role in the genesis of myocardial damage. Since adrenaline increases coronary blood flow small doses of adrenaline in subjects with hypokalaemia may lead to the development of myocardial injury not associated with ischaemia.