高温、亚低温对大鼠脑缺血再灌注损伤的作用及其机制研究

THE STUDY ON EFFECT AND ITS MECHANISM OF HYPERTHERMIA AND MILD HYPOTHERMIA ON ISCHEMIA/REPERFUSIVE IN JURY IN THE CEREBRAL OF THE RATS

目的 :研究轻度高温、亚低温对大鼠脑缺血再灌注损伤组织兴奋性氨基酸 (EAA )与氧自由基的相互关系及病理损伤程度的影响。方法 :6 0只 Wistar大鼠按不同脑温条件随机分为生化组 (n =2 8)和病理组 (n =32 ) ,采用改良 Nagasawa局灶脑缺血再灌注模型 ,观察脑缺血再灌注损伤组织谷氨酸 (Glu)、超氧化物歧化酶 (SOD)、丙二醛 (MDA )的变化及光镜、电镜下的病理变化。结果 :轻度高温明显加重常温脑缺血再灌注损伤组织 Glu、MDA的升高 (P <0 .0 1)及 SOD的下降 (P <0 .0 5 ) ,加重常温脑缺血再灌注组织病理损伤程度 ;亚低温的作用则相反。结论 :轻度高温可能通过同时促进 EAA合成、释放和氧自由基生成系统活化 ,造成大鼠脑缺血再灌注组织损伤加重 ;亚低温可能通过同时抑制 EAA合成、释放和氧自由基生成系统活化 ,减轻大鼠脑缺血再灌注组织损伤程度 ,对大鼠脑缺血再灌注损伤组织起保护作用。

Objective: To study the influence of the relation beteen the excitable amino acid and the free radials and the influence of the pathological injury degree in the cerebral ischemia/reperfusive injury while the injury is developped under the condition of mild hypertherma or mild hypothema Methods: At the different temperatures of the brains of the rats,60 Wistar rats were randomly dievided into two groups: one was the biochemical group(n=28) the other was the pathological group(n=32)  With the improved Nagasawa partial cerebral ischemia/reperfusive model,the change of the content of Glu,SOD,MDA and the pathological change under optic and electric microscope were studied Results: The mild hyperthermia has the effect of increasing the content of Glu, MDA (P<0 01), decreasing the content of SOD(P<0 05) in the ischemia cerebral tissue and increasing pathological injury degree of the cerebral ischemia/reperfusive tissue under the normal temperature condition; but compared with the effect mentioned above, mild hypothermia has the contrast effect Conclusions: The mild hyperthermia increases the injury of ischemia/reperfusive cerebral tissue by promoting the production and the release of the excitable amino acid(EAA) and activation of the system producing free radials;The mild hypothermia decreases the injury degree and protect the ischemia/reperfusive cerebral tissue of the rats by inhibitting the release and production of EAA and activation of the system producing free radials