Twenty-one female dogs (15 mongrel dogs and 6 beagles) were divided into three groups: Midazolam 0.1 mg/(kg h) infusion group (M, n = 7), Propofol 2 mg/(kg h) infusion group (P2, n = 7), Propofol 4 mg/(kg h) infusion group (P4, n = 7). Normothermic ventricular fibrillation (VF) was induced in all dogs for 15 min, followed by brief ECLHA and 168 h of intensive care. The drug infusion was initiated at a constant rate after the restoration of spontaneous circulation (ROSC) to 24 h. Mild hypothermia (33 °C) was maintained for 20 h. Neurological deficit scores (NDS: 0 % = normal, 100 % = brain death) were evaluated for neurological function from 33 to 168 h.
One dog in the M group died, and the remaining dogs survived for 168 h. The P4 group showed better neurological recovery compared with the M group (48 h, 21 ± 16 % versus 32 ± 15 % ; 72 h, 7 ± 6 % versus 25 ± 11 % ; 96 h, 6 ± 6 % versus 21 ± 6 % ; 120 h, 5 ± 5 % versus 20 ± 6 % ; 144 h, 4 ± 4 % versus 20 ± 6 % ; 168 h, 4 ± 4 % versus 20 ± 6 % , p < 0.05). One dog in the P2 and three dogs in the P4 group achieved full neurological recovery (NDS: 0 % ). The number of intact pyramidal cells in the hippocampal CA1 was greater in the propofol groups than midazolam group (p < 0.05).
The combination of propofol infusion at a rate of 4 mg/(kg h), 24 h and rapidly induced mild hypothermia (33 °C) with ECLHA might provide a successful means of cerebral resuscitation from CA.