Neuroprotection Mechanism of Lidocaine in Rabbits with Early Brain Injury Resulted from Subarachnoid Hemorrhage

Abstract

To determine the neuroprotection mechanism of lidocaine on early brain injury resulted from subarachnoid hemorrhage. Methods Eighteen New Zealand white rabbits were randomly divided into three groups: Sham group, subarachnoid hemorrhage (SAH) group and lidocaine treatment (LD) group. Operations were performed on all animals under anesthesia. Autologous nonheparinized arterial blood (1 mL/kg，body mass) was injected into cisterna magna of rabbits in the SAH and LD groups, while saline (1 mL/kg，body mass) was given to rabbits in the sham group. Thirty minutes later, intravenous injection of 0.6 mL 20 mg/mL lidocaine was given to those in the LD group, and intravenous injection of 0.6 mL saline was given to those in the Sham and SAH groups. Food intake and neurological impairments of the rabbits were assessed 72 h after the induction of SAH. The protein and mRNA experssions of Caspase-3 and cytochrome-c (Cyt-c) in hippocampus tissues were detected using real-time PCR （RT-PCR） and Western blot. Results Rabbits in the SAH and LD groups had lower food intake and higher mRNA and protein expressions of Caspase-3 and Cyt-c than those in the sham groups, which was accompanied with varying degrees of neurological impairments. No significant differences in food intake and neurological impairments were found between the SAH and LD groups (P >0.05). However, rabbits in the LD group had lower levels of mRNA and protein expressions of Caspase-3 and Cyt-c than those in the SAH group (P <0.05). Conclusion The neuroprotection mechanism of lidocaine on early brain injury in rabbits with subarachnoid hemorrhage may be associated with inhibition of mitochondrial pathway and downregulated mRNA and protein expressions of Caspase-3 and Cyt-c in brain tissues.

Keywords: Lidocaine, Subarachnoid hemorrhage, Early brain injury, Mitochondrial pathway