大鼠实验性脑出血后高血糖对血肿周围脑组织乳酸与氧自由基的影响

摘要

Objective To observe the effect of post-ICH hyperglycemia on the level of lactic acid and oxygen free radicats in brain tissue around hemotoma and to explore the relative mechanism. Methods The intracerebral hemorrhage (ICH) rat model was established by autologous blood injection, SD rats were randomly divided into sham operation group (SO), pure cerebral hemorrhage (PCH), post-ICH hyperglycemia group by 2g/kg injection of glucose (2-IG), and 4g/kg injection glucose (4-IG). We observed 0, 1, 6 h blood glucose and 0,1,3, 7,10, 14 d perihematoma LA, SOD, MDA content Results 1, 6 h blood glucose values was significantly higher (P＜0. 05) in 2-IG group and 4-IG group than in SO group. LA and MDA of rat brain tissue surrounding hematoma were significantly higher (F＜0.05) and SOD was lower (P＜0.05) in 2-IG and 4-IG group than in PCH group. Conclusions Hyperglycemia after cerebral hemorrhage leads to lactate and MDA accumulation and to the decreased SOD, possibly through free radical chain reaction.%观察大鼠脑出血(ICH)后高血糖对血肿周围脑组织乳酸(LA)和氧自由基的影响,探讨ICH后高血糖加重脑损伤的可能机制.采用自体血注入法建立ICH模型,将SD大鼠随机分成假手术组(SO)、单纯脑出血组(PCH)、ICH后高血糖组,ICH后高血糖组又分为2g/kg(2-IG)和4g/kg(4-IG)注射葡萄糖组.观察各组大鼠术前和术后1、6h血糖变化；测定各组大鼠术后1、3、7、10、14d血肿周围脑组织LA、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量变化. 结果与SO组比较,2-IG组和4-IG组术后1、6h血糖明显升高(P＜0.05)；与PCH组比较,2-IG组和4-IG组大鼠血肿周围脑组织LA和MDA含量明显升高(P＜0.05),SOD含量明显降低(P＜0.05). 结论 脑出血后高血糖导致能量代谢障碍,LA蓄积甚至中毒,可能通过氧自由基连锁反应加重脑损伤.