摘要
①目的 探讨内皮素 - 1 (ET - 1 )对实验性大鼠肢体缺血再灌注 (LIR)后脑损伤的影响及其作用机制。②方法 实验用Wistar大鼠 ,随机分为 7组 ,即 :对照组 (Control) ,缺血组 (I) ,缺血再灌组 (IR) :包括IR 0 .5、2、4、6、1 0小时 5组。分别测定各组动物血浆ET - 1、丙二醛 (MDA)、黄嘌呤氧化酶 (XOD)、超氧化物歧化酶 (SOD)、乳酸脱氢酶 (LDH)、肌酸磷酸激酶 (CK)及脑组织ET - 1、MDA、XOD、SOD、髓过氧化物酶 (MPO)、湿干重比 (W /D)的变化。③结果 LIR后血浆及脑组织ET - 1含量增加 ,在IR4小时达到最高 ,以后稍有下降。血浆中MDA、LDH、CK和脑组织MDA、MPO、W/D增加 ,SOD活性降低。④结论 肢体缺血再灌注后脑损伤的发生与ET -
Objective To evaluate the possible role of endothelin-1 in the development of brain injury after hind limbs ischemia-reperfusion(LIR).Methods Wistar rats were divided into 7 goups : Control group, ischemia group(I), ischemia-reperfusion group(IR)including five groups: IR 0.5h?IR2h?IR4h?IR6h?IR10h group. The changes of Endothelin-1(ET-1)?malondialdehyde (MDA)?xanthine oxidase(XOD)?superoxide dismutase (SOD)?actate dehydrogenase (LDH) and creatine kinase (CK) in plasma were observed.The content of ET-1?MDA?XOD?SOD?myeloperoxidase(MPO) ?W/D in the brain tissue were detected. Results The content of ET-1 in plasma and brain tissue increased following LIR, which were maximal in IR4h,then decreased. The content of MDA?XOD?LDH?CK in plasma and MDA?XOD?MPO?W/D in brain tissue also increased, the activation of SOD decreased. The development of ET-1 may correctly reflect the changes of brain injury. Conclusion The increased of ET-1 after LIR might be the main factor of causing brain injury.
出处
《华北煤炭医学院学报》
2004年第3期278-280,共3页
Journal of North China Coal Medical College