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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。方法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、6 h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、6 h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。
Objective To observe the effect of hyperglycemia on cerebral lactic acid (LA) and oxygen free radical in rats after intracerebral hemorrhage (ICH) and to explore the possible mechanism of hyperglycemia aggravating brain injury after ICH. Methods The ICH model was established by autologous blood injection. The SD rats were randomly divided into sham operation group (SO), PCH group, hyperglycemia group after ICH, hyperglycemia group after ICH and 2g / kg -IG) and 4g / kg (4-IG) glucose group. The changes of blood glucose of the rats in each group were observed before and after 1, 6 h. The levels of LA, SOD, Aldehyde (MDA) content changes. Results Compared with SO group, the blood glucose of 2-IG group and 4-IG group were significantly increased at 1 and 6 h after operation (P <0.05). Compared with PCH group, The levels of LA and MDA were significantly increased (P <0.05) and the content of SOD was significantly decreased (P <0.05). Conclusions After cerebral hemorrhage, hyperglycemia leads to energy metabolism disorder, LA accumulation or even poisoning, which may aggravate brain injury through oxygen radical chain reaction.