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目的观察大鼠脑出血(ICH)后高血糖对血肿周围脑组织NO和三磷酸腺苷(ATP)的影响,探讨ICH后高血糖对脑损伤的可能机制。方法采用自体血注入法建立脑出血模型,将SD大鼠随机分成假手术组(SO)、单纯脑出血组(PCH)、脑出血后高血糖组,脑出血后后高血糖组又分为2 g/kg(2G组)和4g/kg(4G组)注射葡萄糖组,并观察各组大鼠术前、术后1、6 h血糖变化;测定各组大鼠术后1、3、7、10、14 d血肿周围脑组织NO和三磷酸腺苷(ATP)含量变化。结果与SO组比较,脑出血3组血肿周围脑组织NO含量升高,ATP含量降低(P<0.05);与PCH组比较,2G组和4G组大鼠血肿周围脑组织NO含量明显升高(P<0.05),ATP含量明显降低(P<0.05),以4G组变化更明显(P<0.05)。结论脑出血后高血糖可能通过NO的毒性作用加重能量代谢障碍,而加重脑损伤。
Objective To investigate the effects of hyperglycemia on the expression of NO and ATP in rat brain after intracerebral hemorrhage (ICH) and to explore the possible mechanism of hyperglycemia on brain injury after ICH. Methods The model of intracerebral hemorrhage was established by autologous blood injection. The SD rats were randomly divided into sham operation group (SO), simple cerebral hemorrhage group (PCH), hyperglycemia group after intracerebral hemorrhage, and hyperglycemia group after intracerebral hemorrhage (group 2G) and group 4g / kg (group 4G). The changes of blood glucose of the rats in each group were observed at 1, 6 h after operation. The rats in each group were sacrificed at 1, 3, 7, Changes of NO and ATP content in brain tissue around hematoma on the 10th and 14th day. Results Compared with SO group, the content of NO in cerebral hemorrhage group increased and the content of ATP decreased (P <0.05). Compared with PCH group, NO content in brain tissue around 2GH group and 4G group increased significantly P <0.05), ATP content decreased significantly (P <0.05), and the change in 4G group was more obvious (P <0.05). Conclusions After intracerebral hemorrhage, hyperglycemia may aggravate energy metabolism disorder through the toxic effect of NO, which may aggravate brain injury.