Effects of Brain Injury and Anesthertics on Survival Rate Following Brain Ischemia in Mice

Although brain resuscitation measures for the ischemic-anoxic brain injury have been reported inrecent years, none of these is promising in clinical practice. Intrinsic protective mechanisms can be provided in artifically injured brain. The administration of exogenous nerve growth facter (NGF) inhibits naturally occurring cholinergic neuronal death and promote neuronal survival in the sympathetic ganglia after axotomy. Thus, we examined the protective effect of brain injury and anesthetics, on brain ischemia induced by common carotid artery clipping in mice. Mice were randamly dvided in to 3 groups, the anesthesia group, sham operated group (received surgical incision on the scalp without brain injury) and brain injury group. The brain injury was induced by vertically inserting a 25 gauge hypodermic needle 5mm in depth from the skull into the brain at 4 sites. One week after the brain injury, incomplate brain ischemia was applied for 60 min under pentobarbital (80mg/kg) anesthesia or for 30 min under ketamine (200mg/kg) anesthesia. The survival rate was calculated following brain ischemia in each group up to the 7th postischemic day. The survival rate in the brain injury group in which brain ischemia was produced under pentobarbital anesthesia was significantly higher than in the other groups. Improvement of survival rate in mice with brain injury, however, became insignificant when brain ischemia was imposed during ketamine anesthesia. The results suggest that antiischemic factors are released by the injured brain or that certain unknown protective mechanisms against ischemia become active following brain injury during barbiturarate anesthesia. By contrast, an opposing mechanism might develop under ketamine anesthesia, in which protective effects of brain injury against brain ischemia are masked