Mechanism of anodal stimulation of cardiac tissue

The mechanism of end-diastolic anodal stimulation of cardiac tissue did not receive clear experimental interpretation. According to bidomain model theory, anodal stimulation gives rise to make excitation from two regions of induced depolarization (virtual cathode) which surround along fibre the hyperpolarized region at the pacing site (virtual anode). Furthermore, upon termination during diastole of a stimulus pulse initiated in the refractory period of a previous beat, anode break excitation propagates from the hyperpolarized region as a result of depolarization diffusing from the region of the virtual cathode. Nevertheless, anode break response can be readily elicited in single ventricular cells by the recruitment of the hyperpolarisation-activated inward current if which slowly deactivates upon release of the hyperpolarisation. To determine whether anodal stimulation of cardiac tissue has also a cellular basis, we measured unipolar potentials in in vivo rat hearts by means of high spatial resolution electrode arrays. Suprathreshold stimuli gave rise to impulse initiation, 3-5 ms from stimulus onset, at one or two adjacent regions from the pacing site (virtual cathode), suggesting anode make excitation. By a gradually decreasing pulse strength towards threshold, excitation suddenly initiated in the region of the pacing site with a progressively increasing latency of 6-12 ms, suggesting anode break excitation induced by active cellular properties. Current pulses below 0.3 ms gave only rise to anode make excitation at a much higher threshold and the strength-duration curve rapidly increased its slope in this interval. The results indicate that anode break excitation can originate at the site of stimulation itself at a lower threshold than that of make excitation from adjacent regions of induced depolarization, with a mechanism induced by active cellular properties.