出血性脑梗死大鼠脑损伤机制及三磷酸腺苷敏感性钾通道的作用

Mechanism for brain injury of hemorrhagic infarction in rats and roles of adenosine triphosphate sensitive potassium channels

目的:验证KATP通道是否参与出血性脑梗死的病理过程,探讨HI继发脑损伤的机制.方法:健康雄性Spra-gue-Dawley大鼠96只,随机分为出血性脑梗死(hemorrhagic infarction,HI)组、单纯脑梗死(cerebral infarction,CI)组、格列苯脲(Glibenclamide,Gli)干预(Gli+HI,GH)组和假手术(Sham)组.应用两步法建立HI大鼠模型.术后3,6,12,24h进行神经功能评分、脑组织含水量及脑组织三磷酸腺苷酶(adenosine triphosphatase,ATPase),琥珀酸脱氢酶(succinic dehydrogenase,SDH),丙二醛(malondialdehyde,MDA)测定.结果:HI组和CI组大鼠术后各时间点神经功能评分、脑组织含水量差别无统计学意义(P>0.05).HI组大鼠脑组织AT-Pase活性术后12,24h高于CI组(P<0.05),SDH活性术后24h高于CI组(P<0.05),MDA含量术后12h低于CI组(P<0.05);以上现象均可被Gli取消.结论:应用两步法制作的HI大鼠模型较为稳定、可行.CI后继发中等量出血后早期,脑组织对缺血缺氧耐受性增强,延缓了脑损伤,与KATP通道开放有关.

AIM： To determine whether adenosine triphosphate sensitive potassium（ KATP ） channels participates in the histological progress of hemorrhagic infarction（HI） and to explore the mechanism of brain injury following HI. METHODS： Ninety-six healthy male Sprague-Dawley rats were divided randomly into HI group, cerebral infarction（CI） group, Glibenclaimide（Gli） ＋ HI （GH） group and sham operation group. Two-step method was used to develop the HI model in rats. Then changes in neurobehaviour, brain water content, brain adenosine triphosphatase（ AT- Pase） activity, succinic dehydrogenase （SDH） activity and malondialdehyde（MDA） content were measured at 3,6,12 and 24 hours after operation. RESULTS： On neurobehavioral deficit and brain water content test, HI group presented no aggravation com- pared with CI group （ P 〉 0.05 ）. Brain ATPase activity of HI group was higher than that of CI group at 12 and 24 h （P 〈 0.05 ）. Brain SDH activity of HI group was higher than that of CI group at 24 h （ P 〈 0.05 ）. And brain MDA content of HI group was lower than that of CI group at 12 h （ P 〈 0.05 ）. All the above-mentionod changes were cancelled by Gli. CONCLUSION： The HI model in rat established by two-step method is reproducible and stable. A medium volume of hemorrhagic transformation after CI does not aggravate the brain injury at early stage, in which KATP channels play an important role.