Kr K1 three cell types have also been shown to possess different be homogeneously distributed across the ventricular wall pharmacologic profiles and to respond differently to a of the canine heart. Cells with repolarization characteristics variety of pathophysiologic states [3–8]. of M cells have been described in the canine, guinea pig, The three cells types differ principally with respect to rabbit, pig and human ventricles [3–8, 15, 18–33]. Three repolarization characteristics. Ventricular epicardial and M studies have failed to discern M cells in the ventricles of cells display action potentials with a prominent transient the pig, guinea pig and rat [7, 34, 35]. Other studies, while outward current (I)-mediated phase 1, giving rise to a clearly demonstrating the presence of M cells in the to notched appearance of the action potential. The absence of ventricles of the canine heart in vitro, failed to delineate a prominent notch in the endocardium is a consequence of the unique cell type in vivo [23, 36]. Methodological a much smaller I. Similar regional differences in I are considerations thought to be responsible for these differ-to to found in canine, feline, rabbit, rat and human ventricular ences have been discussed at great length [1, 2]. myocytes (see [1] for references). Recent studies also When individual myocytes are enzymatically dissociated indicate that I and the action potential notch are much from the respective layers of the canine left ventricular to larger in right vs. left ventricular epicardial [9] and M [10](LV) wall, transmural dispersion of action potential duracells. The transmural gradient in the amplitude of the tion (TD-APD) recorded at slow rates is of the order of I-mediated action potential notch underlies the normal J approximately 200 ms. When these cells are in the intact to wave or J point elevation in the ECG [11] and its wall of the LV, this intrinsic dispersion is greatly reduced accentuation, particularly in the right ventricle, contributes due to electrotonic interactions among the different cell to the development of life-threatening arrhythmias in types. Studies conducted in perfused canine LV wedge patients with the Brugada syndrome and various forms of preparations generally display TD-APD values ranging idiopathic ventricular fibrillation [12, 13]. The presence of a between 40 and 60 ms at slow rates (basic cycle length prominent I in right ventricular epicardium has also been[BCL] 52000 ms), depending on the size of the heart. At to shown to sensitize this tissue to the effects of ischemia faster rates, TD-APD is further reduced. Transmural [14]. Accentuation of the action potential notch and dispersion of repolarization (TDR) averages 34618 ms at eventual loss of the dome in right ventricular epicardium a BCL of 1000 ms [31]. but not endocardium has been shown to contribute to In addition to disparities in the time of final repolarizaischemia-induced ST segment elevation [12]. tion, there are important differences in the voltage of the The M cells are distinguished by the ability of their action potential plateau, which can only be discerned using action potentials to prolong more than those of epicardium intracellular microelectrode techniques. These differences in the trajectory of repolarization are responsible for the inscription of the electrocardiographic T wave. Data from