We determined the threshold for ventricular fibrillation by means of sinusoidal alternating current (AC) from 1 to 1000 Hz on isolated perfused guinea pig hearts. Current was applied via electrodes located in the aorta and at the apex of the heart. The duration of current flow was kept constant at 1 s. Electrical activity was recorded with epicardial electrodes attached to the ventricles. Additional experiments were performed in isolated papillary muscles with intracellular microelectrodes. The fibrillation threshold, expressed as peak-to-peak current strength, attains a minimum at about 30 Hz and rises by a factor of 5 at 1 Hz, and by a factor of 14 at 1000 Hz. In the frequency range from 30 to 1000 Hz the rise of the fibrillation threshold can be attributed to the increase of the threshold for stimulation due to the progressive shortening of the AC periods. Thus no change of the fibrillation threshold occurs if DC pulses of constant duration are used in the same range of frequencies. Below 30 Hz there is only a slight increase of the threshold for stimulation, which cannot entirely account for the rise of the threshold for fibrillation. A likely cause of the reduced susceptibility of the heart to fibrillation at the lower frequencies is the reduced number of extrasystoles preceding the onset of fibrillation, which results in a less pronounced state of inhomogeneous excitability.
Isolated perfused guinea pig hearts (Langendorff preparation) were arrested by carbachol (0.1-0.2 mg/l) and electrically stimulated in the region of the av-conducting system. The QT interval was determined by means of extracellular electrodes at different driving frequencies. Separate experiments were performed on papillary muscles from the right ventricle to measure the duration of the transmembrane action potential under comparable conditions. At 35 degrees C (Ke+ 5.4 mmol/l) increasing the frequency of stimulation (range 12-120/min) caused the action potential duration (APD) to decrease to a greater extent than the QT interval. Stepwise rising of the external K+ concentration up to 16.2 mmol/l produced a nearly parallel shift to the APD-frequency relation to lower values. Again, the QT interval was less affected by increasing the external K+ concentration than the APD. Stepwise reduction of the temperature down to 20 degrees C prolonged the APD as well as the QT interval, the effects being more pronounced at lower than at higher stimulation frequencies. Under all examined experimental conditions, the APD proved to be markedly shorter than the QT interval even when the latter is diminished by the duration of QRS. The results suggest that no close relation exists between the APD and the QT interval. The observed divergencies may be due to functional differences among various parts of the ventricles.
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