摘要
BACKGROUND： Abnormal changes in magnesium ion are closely related to cerebral injury. At present, some evidence indicates that magnesium reagent can improve nerve function and prognosis of patients with cerebral injury. OBJECTIVE： To observe the effect of magnesium sulfate on changes in nitric oxide synthase （NOS） activity in brain tissue of rats with acute craniocerebral injury. DESIGN： Completely randomized grouping design and randomly controlled study. SETTING： Laboratory of Neurosurgery, the Third Hospital of Chinese PLA. MATERIALS： Fifty-four male SD rats of clean grade and weighing 220 - 250 g were randomly divided into normal control group （n =6）, cerebral injury group （n =24） and magnesium sulfate group （n =24）. Especially, rats in cerebral injury group and magnesium sulfate group were equally divided into four subgroups and observed at 0.5, 2, 6 and 24 hours after model establishment. A solution of 125 g/L of magnesium sulfate was provided by the Seventh Pharmaceutical Factory of Wuxi and the NOS assay kit by Nanjing Jiancheng Bioengineering Institute. METHODS： The experiment was carried out in the Institute of Neurosurgery, the Third Hospital of Chinese PLA from August 2000 to August 2002. ① Rats in the cerebral injury group and magnesium sulfate group were anesthetized to establish cerebral injury models based on modified Feeney technique; magnesium sulfate group were intraperitoneally injected 600 mg/kg magnesium sulfate （125 g/L）, but rats in the normal control group remained untreated. ② At 0.5, 2, 6 and 24 hours after cerebral injury, rats in cerebral injury group and magnesium sulfate group were decapitated and brains were dissected. Cerebral cortex of rats in cerebral injury group was selected for NOS assay; in addition, at 0.5 hour after cerebral injury, a portion of the parietal lobe was selected from the brains of rats in the normal control group. Brain samples were homogenized, the homogenated centrifuged and the supernatants were used to measure NOS activity with NOS kit. ③ Differences among the three groups were compared with t test. MAIN OUTCOME MEASURES： NOS activity in cerebral cortex of rats in each group. RESULTS： A total of 54 SD rats were involved in the final analysis. At 0.5 hour after cerebral injury, NOS activity in cerebral cortex was （42.45 ± 13.46） nmol/L in cerebral injury group and （41.17 ± 12.53） nmol/L in magnesium sulfate group, respectively, which was higher than that in normal control group [（39.45 ± 11.84） nmol/L, P 〈 0.05]. At 2 hours after cerebral injury, NOS activities were （66.48 ±21.43） and （63.24 ± 19.18） umol/L, respectively, while at 6 hours after cerebral injury, NOS activities were （62.45 ± 24.18） and （51.97 ±20.46） nmol/L, respectively, which were higher than those in normal control group （P 〈 0.0 1）. At 24 hours after cerebral injury, NOS activity returned to basal level. Moreover, NOS activity was significantly lower in the magnesium sulfate group than that in the cerebral injury group at 2 and 6 hours after cerebral injury （P 〈 0.05, 0.01）.CONCLUSION： NOS activity is increased in injured brain tissue of rats with craniocerebral injury, and treatment with magnesium sulfate provides some degrees of protection possibly through inhibition of NOS activity after cerebral injury.
BACKGROUND： Abnormal changes in magnesium ion are closely related to cerebral injury. At present, some evidence indicates that magnesium reagent can improve nerve function and prognosis of patients with cerebral injury. OBJECTIVE： To observe the effect of magnesium sulfate on changes in nitric oxide synthase （NOS） activity in brain tissue of rats with acute craniocerebral injury. DESIGN： Completely randomized grouping design and randomly controlled study. SETTING： Laboratory of Neurosurgery, the Third Hospital of Chinese PLA. MATERIALS： Fifty-four male SD rats of clean grade and weighing 220 - 250 g were randomly divided into normal control group （n =6）, cerebral injury group （n =24） and magnesium sulfate group （n =24）. Especially, rats in cerebral injury group and magnesium sulfate group were equally divided into four subgroups and observed at 0.5, 2, 6 and 24 hours after model establishment. A solution of 125 g/L of magnesium sulfate was provided by the Seventh Pharmaceutical Factory of Wuxi and the NOS assay kit by Nanjing Jiancheng Bioengineering Institute. METHODS： The experiment was carried out in the Institute of Neurosurgery, the Third Hospital of Chinese PLA from August 2000 to August 2002. ① Rats in the cerebral injury group and magnesium sulfate group were anesthetized to establish cerebral injury models based on modified Feeney technique; magnesium sulfate group were intraperitoneally injected 600 mg/kg magnesium sulfate （125 g/L）, but rats in the normal control group remained untreated. ② At 0.5, 2, 6 and 24 hours after cerebral injury, rats in cerebral injury group and magnesium sulfate group were decapitated and brains were dissected. Cerebral cortex of rats in cerebral injury group was selected for NOS assay; in addition, at 0.5 hour after cerebral injury, a portion of the parietal lobe was selected from the brains of rats in the normal control group. Brain samples were homogenized, the homogenated centrifuged and the supernatants were used to measure NOS activity with NOS kit. ③ Differences among the three groups were compared with t test. MAIN OUTCOME MEASURES： NOS activity in cerebral cortex of rats in each group. RESULTS： A total of 54 SD rats were involved in the final analysis. At 0.5 hour after cerebral injury, NOS activity in cerebral cortex was （42.45 ± 13.46） nmol/L in cerebral injury group and （41.17 ± 12.53） nmol/L in magnesium sulfate group, respectively, which was higher than that in normal control group [（39.45 ± 11.84） nmol/L, P 〈 0.05]. At 2 hours after cerebral injury, NOS activities were （66.48 ±21.43） and （63.24 ± 19.18） umol/L, respectively, while at 6 hours after cerebral injury, NOS activities were （62.45 ± 24.18） and （51.97 ±20.46） nmol/L, respectively, which were higher than those in normal control group （P 〈 0.0 1）. At 24 hours after cerebral injury, NOS activity returned to basal level. Moreover, NOS activity was significantly lower in the magnesium sulfate group than that in the cerebral injury group at 2 and 6 hours after cerebral injury （P 〈 0.05, 0.01）.CONCLUSION： NOS activity is increased in injured brain tissue of rats with craniocerebral injury, and treatment with magnesium sulfate provides some degrees of protection possibly through inhibition of NOS activity after cerebral injury.
