Abstract 468 Emergency Medicine II Platform, Monday, 5/3

A spontaneous reduction in core temperature occurs after asphyxial cardiac arrest in rats. To determine if spontaneous hypothermia influences neurologic damage after asphyxial arrest, we compared neurologic outcome in rats permitted to develop spontaneous hypothermia vs. rats managed with controlled normothermia.

Male, Sprague Dawley rats (n = 31) were anesthetized, intubated, paralyzed and then disconnected from the ventilator for 8 min (2.5 min of asphyxiation followed by 5.5 min of cardiac arrest). Following 8 min of asphyxia, rats were resuscitated with chest compressions, epinephrine, sodium bicarbonate, and ventilation was resumed. Rats were extubated one h post-resuscitation. Tympanic membrane temperature was maintained at 37.4° C during the preparation, insult, and the one h interval prior to extubation. Following extubation, 14 rats (Group 1) were returned to a temperature-controlled room (23.3° C) while 9 rats (Group 2) were housed separately for 48 h in servo-controlled incubators set to maintain rectal temperature at 37.4° C. Neurologic outcome was assessed daily with a neurodeficit score (NDS; 0-100, 0 =normal). Rats were sacrificed at 72 h and H&E stained brain-sections were examined by a pathologist blinded to group. Histopathology was scored for 40 brain regions using a five-point ordinal scale (0 = none, 5 = severe).

Mortality (death prior to 72 h sacrifice) was lower in Group 1 compared to Group 2 (0/14 vs. 3/9; p = 0.05, Fischer exact test)and Group 1 demonstrated a more favorable progression in NDS (10 ± 9 vs. 40 ± 19 at 72 h; p < 0.05). Similarly, median histopathology scores were lower (less injury) in Group 1 compared to Group 2 for temporal cortex (0 vs. 2.5), parietal cortex (0 vs. 2), thalamus (0 vs. 3), CA1 hippocampus (1.5 vs. 4.5), CA2 hippocampus (0 vs. 3.5), subiculum (0 vs. 4), and cerebellar purkinje cell layer (2 vs. 4) (all p < 0.05).

After demonstrating an improvement in mortality, NDS, and histopathology in asphyxiated rats allowed to develop spontaneous hypothermia, we sought to characterize the time course and extent of the hypothermia. Accordingly, a cohort of 8 asphyxiated rats (Group 3) were returned to a temperature-controlled room (23.3° C) with continuous monitoring of rectal temperature. Mean rectal temperatures were 36.5, 34.8, 34.5, 35.2, and 36.7, at 2, 8, 12, 24, and 36 h respectively.

We conclude that rats resuscitated from asphyxial cardiac arrest develop delayed, prolonged hypothermia that is neuroprotective.

Supported by Children's Hospital of Pittsburgh