On the mechanism of idioventricular pacemaker suppression by fast drive.
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Biomedical subjects
Publications and source records attributed to M B Pliam.
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The influence of norepinephrine on ventricular overdrive suppression and attendant potassium shifts has been studied in isolated perfused canine hearts with complete atrioventricular block. It was found that: 1) there is a potassium loss during the drive and a potassium uptake after the drive); 2) reducing the driving rate from 240 to 120/min decreases potassium loss; 3) norepinephrine increases potassium uptake and spontaneously beating ventricles and during the recovery from 120/min drive; 4) norepinephrine enhances K loss during and after a 240/min drive; 5) norepinephrine shortens the overdrive pause under all the conditions tested; 6) in ventricles driven at a constant rate, norepinephrine causes a small loss of ptoassium; 7) reserpinized hearts show a small potassium loss during drive and a larger potassium uptake after drive; yet, the suppression is longer; 8) norepinephrine increases K loss with drive and decreases overdrive suppression in reserpinized hearts; 9) norepinephrine enhances the increase in oxygen consumption caused by overdrive; and 10) norepinephrine antagonizes the depressant effect of high [K]0 on automaticity. It is concluded that norepinephrine shortens the pause independently of potassium levels and antagonizes the inhibittory influence of high K. The effect or norepinephrine on K movements depends on the ventricular rate and such rate-dependence is related to oxygen availability with respect to the increased metabolic demand.