Inhibitory effects of lidocaine on cerebral vasospasm in a rabbit model of subarachnoid hemorrhage

Following subarachnoid hemorrhage, vasoconstrictor substances, cellular apoptosis, blood coagulation, and vascular cell proliferation affect the onset of cerebral vasospasm. Previous studies from our laboratory have revealed that injection of lidocaine (2 mg) into the cisterna magna reduces cerebral vasospasm and nerve functional impairment in an animal model of subarachnoid hemorrhage. The present study determined the optimal lidocaine dose for vasospasm and brain injury by injecting different doses of lidocaine into the cisterna magna in a rabbit model of subarachnoid hemorrhage. Results showed that endothelin, tumor necrosis factor-α, and interleukin-6 levels significantly increased in plasma, and calcitonin gene-related peptide levels significantly decreased in plasma (P < 0.05). The number of neurons was decreased, the number of cells expressing c-Fos increased in the hippocampus, and cross-sections and diameters of basilar arteries were reduced (P < 0.05). These changes significantly improved following injection of lidocaine (1, 2, 4, and 6 mg) into the cisterna magna. A dose of 6 mg lidocaine into the cisterna magna resulted in optimal effects on cerebral vasospasm and brain injury following subarachnoid hemorrhage.