Table 1.
Type | Species/CellType | Reference |
---|---|---|
A | Mouse heart | Killeen et al. (41) |
A | Rat papillary and guinea pig ventricle | Aomine et al. (2), Fedida et al. (20), Miura et al. (59) |
B | Rat and guinea pig ventricle | Beresewicz and Horackova (4) |
B | Guinea pig atrial cells | Song et al. (84) |
B | Rabbit ventricle | Wu and Corr (104), Wongcharoen et al. (103) |
B | Rabbit pulmonary vein | Wongcharoen et al. (102) |
B | Canine ventricle | deGroot et al. (14) |
B | Calf Purkinje cells | Lederer and Tsien (46), Kass and Tsien (40) |
B | Sheep Purkinje cells | Neiman and Eisner (62) |
C | Rat ventricle | Ruocco et al. (78), Xie et al. (105) |
C | Rat atrial cells | Tavi et al. (89) |
C | Guinea pig ventricle | Song and Belardinelli (83), Tweedie et al. (93), Song et al. (85) |
C | Guinea pig heart (in vivo) | Xu and Pelleg (107) |
C | Ferret ventricle | Marban et al. (56) |
C | Canine ventricle | Priori and Corr (76), Laurita and Katra (44) |
C | Canine ventricle wedge | Nam et al. (61) |
C | Canine ventricle and Purkinje cells | Burashnikov and Antzelevitch (7) |
C | Canine atrial and Purkinje cells | Burashnikov and Antzelevitch (8) |
C | Canine atrial cells | Tseng and Wit (92) |
C | Sheep Purkinje cells and ventricle | Verkerk et al. (95) |
C | Human ventricle | Verkerk et al. (94, 96) |
C | Human heart (in vivo) | Chen at al. (9) |
D | Rat ventricle | Nordin et al. (67) |
D | Guinea pig ventricle | Aomine et al. (1) |
E | Guinea pig ventricle | Spencer and Sham (86) |
F | Canine atrial cells | Stambler et al. (87) |
G | Canine Purkinje cells | Levy and Wiseman (47) |
H | Mouse cells | Wehrens (99), Liu et al. (49), Rizzi et al. (77) |
H | RyR2 mutant in human embryonic kidney-293 cells | Jiang (38, 39) |
I | Rabbit ventricle | Schlotthauer and Bers (80) |
Four publications used hypokalemia (type A), nine publications used induced Na+ overload (type B), eighteen publications used increased L-type Ca2+ current (ICaL; mainly via the β-adrenergic pathway; type C), two publications increased extracellular Ca2+ (type D), one publication used hyponatremia and uncaging of Ca2+ (type E), one publication used rapid pacing (type F), and one publication used a combination of these ways (type G) to increase intracellular Ca2+, which then lead to the observation of delay afterdepolarizations (DADs). Five more wet experimental studies used mutations of ryanodine receptors (RyRs; type H) to increase the incidence of DADs. One study used surrogates for DADs (type I) to investigate the relation between Ca2+ load of the sarcoplasmic reticulum (SR) and the ability to induce DADs that trigger full action potentials.