Outcome effects of different protective hypothermia levels during cardiac arrest in rats

Although hypothermia is widely used to protect the brain during cardiac and neurologic surgery, the optimal level of cooling has not been established. This study examined the protective effect of graded levels of surface cooling on cerebral function in rats after complete global cerebral ischemia.

Groups of ketamine-anesthetized rats (13 animals in each group) were cooled to cranial temperatures of 34, 30, 27, 24, or 22 degrees C before circulatory arrest. Also a normothermic (37 degrees C) group was tested. After cooling, an 11-min circulatory arrest was produced by atraumatic chest compression. Circulatory arrest was followed by cardiopulmonary resuscitation and rewarming without postischemic intensive care. On the fifth postinsult day, neurologic outcome was scored on a 50-point neurodeficit scale (NDS 0 = normal). The percent of ischemic pyramidal neurons in the CA1 hippocampal region was also determined.

There were no survivors in the normothermic group. Neurologic recovery was enhanced with 30 degrees C cranial temperature, as compared to outcome in the 34 degrees C group. Further cooling did not change outcome. The neurodeficit scales were significantly lower in all other groups compared to the 34 degrees C group on the fifth postinsult day. The percent of ischemic neurons did not change significantly as a function of cooling, but the lowest count appeared at 27 degrees C.

In this model, moderate (30 degrees C) cooling improved neurologic outcome. There was no additional benefit from more extreme hypothermia.