THE EFFECT OF PAPAVERINE, EPINEPHRINE AND QIJINIDINE ON THE FIBRILLATION THRESHOLD OF THE MAMMALIAN VENTRICLES’

In previous papers, Wiggers and W#{233}gria(1, 2, 3, 4) examined the physiological basis of a new method for determining the fibrillation threshold of the ventricles. Using the same technique, Wiggers, W#{233}gria and Pifiera studied the effect of procaine (4) and coronary occlusion (5) on the fibrillation threshold. Subse-quently W#{233}gria, Geyer and Brown (6) employed the method to study the effect of digitalis and ouabain. As reviewed in this communication, the method con-sists of applying a short D.C. stimulus of constant duration (e.g., 0.02 or 0.03 sec.) directly to the ventricle through non-polarizable electrodes in such a way that it falls during the vulnerable period of the heart cycle, i.e., late in systole or very early in diastole. The strength of such a shock (expressed in M.A.) which is just sufficient to cause the ventricles to fibrillate has been termed the fibrillation threshold shock. In order to study physiological, pharmacological or pathological factors which may influence the fibrillation threshold, it is neces-sary to repeat fibnillations before and after such influences. Consequently, in these experiments the fibrillation of the ventricles was promptly stopped b