Limits to milk flow and energy allocation during lactation of the hispid cotton rat (Sigmodon hispidus)

INTRODUCTION: Epicardial and endocardial defibrillation electrode systems affect myocardial electrophysiology and sympathetic function differently. Thus, we postulate that antiarrhythmic drugs will interact with these electrode systems differently. METHODS AND RESULTS: Defibrillation energy requirements (DER) at 20% (ED20), 50% (ED50), and 80% (ED80) success were measured at baseline and during lidocaine (10 mg/kg per hour) or D5W treatment for epicardial and endocardial electrodes. Pigs were randomized to treatment (lidocaine or D5W) and electrode system, which resulted in four experimental groups: (1) epicardial electrode + D5W; (2) epicardial electrode + lidocaine; (3) endocardial electrode + D5W; and (4) endocardial electrode + lidocaine. ED50 DER (mean +/- SEM) values at baseline for groups 1-4 were 10.6+/-1, 8.5+/-1, 12.6+/-1, and 12.3+/-1 J, respectively. DER values for groups 1 and 3 during D5W were similar to baseline. Conversely, lidocaine increased ED50 DER values from 8.5+/-1 to 13.5+/-2 J (P < 0.05) in group 2 animals (epicardial electrodes). When lidocaine was administered to group 4 animals (endocardial electrodes), however, ED50 DER values remained similar to baseline values (12.3+/-1 to 14.3+/-2 J, P = NS). Lidocaine increased ED50 DER values by 59% with the epicardial electrode system, which was significantly greater than the 16% increase with the endocardial electrode system (P < 0.05). Electrophysiologic response and electrode impedance were similar between electrode systems. CONCLUSION: Lidocaine increases DER values to a greater extent when using epicardial versus endocardial electrode system. Thus, drug-device interactions are dependent on the electrode system. These data suggest that the electrophysiologic milieu created by endocardial defibrillation mitigates the effects that lidocaine has on DER values.