Prevention of postischemic hyperthermia prevents ischemic injury of CA1 neurons in gerbils.

Halothane-anesthetized Mongolian gerbils were submitted to 5-min bilateral carotid artery occlusion. After ischemia, halothane anesthesia was continued for various periods of up to 85 min, and the degree of CA1 neuronal injury was estimated 7 days later by counting the number of surviving pyramidal cells. During ischemia and postischemic halothane anesthesia, rectal and cranial temperature was kept at control level (37.7 and 37.0 degrees C, respectively) using a feedback-controlled heating system. When anesthesia was discontinued after ischemia, transient hyperthermia occurred. In animals with 0- and 15-min postischemic halothane anesthesia, both cranial and rectal temperature rose by approximately 1.5 degrees C, and the number of surviving CA1 neurons amounted to less than 25% of control. After 45- or 85-min postischemic anesthesia, hyperthermia was significantly reduced and the number of surviving neurons increased to 65 and 89%, respectively. The protective effect of postischemic anesthesia was lost when anesthetized animals were submitted to the same hyperthermic profile as nonanesthetized ones, using a feedback-controlled heating system (16% surviving neurons in hyperthermia vs. 89% in normothermia, respectively). These observations demonstrate that postischemic anesthesia with 1% halothane protects against delayed neuronal death by preventing postischemic hyperthermia and not by its anesthetic effects.