Minor Changes in Core Temperature Prior to Cardiac Arrest Influence Outcomes: An Experimental Study

To investigate whether slight variations in core temperature prior to cardiac arrest (CA) influence short-term outcomes and mitochondrial functions.

Three groups of New Zealand White rabbits (n = 12/group) were submitted to 15 minutes of CA at 38°C (T-38 group), 39°C (T-39), or 40°C (T 40) and 120 minutes of reperfusion. A Sham-operated group (n = 6) underwent only surgery. Restoration of spontaneous circulation (ROSC), survival, hemodynamics, and pupillary reactivity were recorded. Animals surviving to the end of the observation period were euthanized to assess fresh brain and heart mitochondrial functions (permeability transition and oxidative phosphorylation). Markers of brain and heart damages were also measured.

The duration of asphyxia required to induce CA was significantly lower in the T-40 group when compared to the T-38 group (P < .05). The rate of ROSC was >80% in all groups (P = nonsignificant [ns]). Survival significantly differed among the T-38, T-39, and T-40 groups: 10 (83%) of 12, 7 (58%) of 12, and 4 (33%) of 12, respectively (log-rank test, P = .027). At the end of the protocol, none of the animals in the T-40 group had pupillary reflexes compared to 8 (67%) of 12 in the T-38 group (P < .05). Troponin and protein S100B were significantly higher in the T-40 versus T-38 group (P < .05). Cardiac arrest significantly impaired both inner mitochondrial membrane integrity and oxidative phosphorylation in all groups. Brain mitochondria disorders were significantly more severe in the T-40 group compared to the T-38 group (P < .05).

Small changes in body temperature prior to asphyxial CA significantly influence brain mitochondrial functions and short-term outcomes in rabbits.