Author + information
- Received July 16, 1982
- Accepted September 21, 1982
- Published online March 1, 1983.
- ↵*Address for reprints: Leonard S. Dreifus, MD, Lankenau Hospital. Lancaster and City Line Avenues, Philadelphia, Pennsylvania 19151.
The size and conductivity of the premature response were compared with those of basic responses in canine ventricular tissue perfused with a high potassium ion (K+) (21 mM), high calcium ion (Ca2+) (10 mM) solution. After eight driving stimuli (S1) of 0.5 Hz, premature stimuli (S2) were applied at variable intervals. Action potentials elicited by S1and S2of equal strength and duration were recorded by conventional microelectrode techniques at proximal and distal points 3 to 6 mm apart. The amplitude and duration of action potentials and interelectrode conduction time were examined. The basic response recorded at proximal points was small (30 ± 6 mV, 34 ± 12 ms) (mean ± standard deviation) and did not conduct to distal points. However, a premature response elicited between 188 ± 58 and 523 ± 107 ms after S1was larger than the basic response and conducted successfully to distal points, although with delay. Its amplitude, duration and conduction velocity decreased progressively as the S1-S2interval was increased further. In addition, in response to increasing the stimulus strength, there was a progressive and marked augmentation of the premature response despite little change in the basic action potential. Verapamil (5 × 10-6g/ml) depressed and isoproterenol (10-7g/ml) augmented both basic and premature responses; augmented premature responses were still observed in the presence of high concentrations of propranolol (10-4g/ml). There was no evidence for either summation or oscillatory potentials as the mechanism involved in this phenomenon. Additional experiments using locally depressed tissue sandwiched between normal tissues revealed that spontaneous repetitive responses were elicited after the augmented premature depolarization, and suggested that the supernormal response could be responsible for the initiation of some cardiac arrhythmias, such as the appearance of a reentrant phenomenon.
- Received July 16, 1982.
- Accepted September 21, 1982.
- American College of Cardiology Foundation