Mechanism of Augmented Premature Responses in Canine Ventricular Muscle

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Abstract

SUMMARY

In an effort to determine the mechanism inducing paradoxical augmentation of the very premature action potential (AP), we performed the folio-wing experiments. Premature stimuli (Si) were applied to isolated canine ventricular muscle at variable intervals after every 10th to 15th driving stimulus (Si) at 0.5-1 Hz. Action potentials (Ri and Ri) elicited by Si and Si of equal strength and duration were recorded by conventional microelectrode methods. Measurements were made of the amplitude (Amp), duration (APD), plateau area (PA), and nunrimnm rising velocity (Vr a) of each AP and the proximity (P), the interval from 90% repolarization point of Ri to Si. In normal K+ solution, Rj had a greater plateau area (PAi) than Ri at P less than 300 msec Moreover, PA increased progressively with decreasing P at [Ca1*], of 0.4, 1.6, and 6.4 DIM and reached its maximum at P of 40-90 msec. The maximum APA [(PAj-PAt)/PAi × 100] was estimated at 15 ± 9, 28 ± 6, and 61 ± 11% at each [Cat+lo, which showed that APA increased significantly (P < 0.01) as the [Ca1*], was increased. Verapamil (10″' M) suppressed completely this augmentation in the plateau of the premature AP. In addition, experiments in high K+ (21 mM)-high Ca*+ (6.4-10 nm) solutions revealed that the Amp, APD, and Vrnn of Ri were greater than those of Ri. They progressively increased with a reduction of the Si-Si interval, just as did the plateau of the premature AP at normal [K+]o-These findings suggest that augmented Ca1*-influx may be triggered by a very premature depolarization in canine ventricular muscle, in contrast to the prevailing concept that recovery from inactivation of the Ca++ current is delayed in mammalian heart muscle. Circ Ret 44: 634-629, 1979

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