Negative inotropic effect of K+: its modification by Ca++ and acetylstrophanthidin in dogs

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Abstract
Infusions of K+ into each of the major coronary arteries of anesthetized dogs produces reversible ecg changes and depression of contractile force in areas perfused by K+. The magnitude of depression of contractile force was related to the rate of K+ infusion but not to the total amount of administered K+. K+ infusions into the left anterior descending artery at a rate of 0.1 [mu]Eq/kg sec. did not depress left ventricular contractile force (LVCF), while infusions at a rate of 1.6 [mu]q/kg per sec consistently depressed LVCF more than 70% and produced ventricular fibrillation. Transient reversible, rate-dependent depression occurred only when the rates of K+ infusion varied between 0.2-0.8 [mu]Eq/kg/sec. K+ infusions into the right coronary artery depressed right ventricular contractile force more than K+ infusions into either major branch of the left coronary artery depressed LVCF at all rates of K+ infusions. The negative inotroplc K+ effect occurred without preceding change of heart rate, increased QRS duration, or change of coronary blood flow. The study did not determine whether the negative inotroplc effect was due to a direct effect of K+ on the contractile system, or was secondary to the effects of K+ on the membrane, because the decrease of contractile force was always associated with currents of injury and shortening of the Q-T interval. The negative inotropic effect of K+ was abolished by the simultaneous administration of equivalent amounts of Ca++. Pretreatment with a maximal nontoxic dose of acetylstrophanthidin did not alter the negative inotropic effect of K+.