Abstract
The electrocardiographic changes produced in rabbits by large doses of vasopressin are interpreted to arise from an initial, unstable, state of apical accelerated repolarisation followed by a more enduring state of subendocardial injury. When rabbits were treated, daily, with a commercial heart extract for two weeks and then given vasopressin two days after treatment had stopped, signs of apical accelerated repolarisation were unaltered but the signs of subendocardial injury were substantially suppressed.