Pigs were randomized to: (1) sham (n = 7), (2) cardiac arrest (CA; n = 16), or 3) cardiac arrest + adenocaine (CA + AL; n = 12). After 7 min of electrically induced ventricular fibrillation, start of CPR was followed by infusion of saline (CA) or adenocaine (CA + AL) for 6 min. Haemodynamics, cardiodynamics (pressure-volume loops) and leucocyte superoxide anion generation were assessed. Neurological function was evaluated after 24 h by histology and neurological deficit score (0 = normal; 500 = brain dead).
Rate of ROSC was comparable between groups: CA group 11/16 and CA + AL group 7/12 p = 0.57). Cardiac index transiently increased after ROSC in both groups. Left ventricular dysfunction demonstrated by a rightward shift of the intercept of end-systolic pressure-volume relations in CA was avoided in the CA + AL group. Leucocyte superoxide anion generation 2 h after ROSC was significantly attenuated in the CA + AL group compared to the CA group. Neurological deficit scores [CA: median: 17.5(IQR:0-75) and CA + AL: 35(IQR:15-150)] and histopathological damage were comparable in both groups (p = 0.37).
Infusion of adenocaine during early resuscitation from CA significantly improved early post-resuscitation cardiac function and attenuated leucocyte superoxide anion generation, without a change in post-ROSC neurological function. (IACUC protocol number 023-2009).