冷损伤血管脂质过氧化水平的变化及其意义

Changes of lipid peroxidation(LPO) in cold injured blood vessels

目的 探讨自由基在血管冻结损伤发生中的作用及其对制定治疗措施的意义。方法 分离Wistar大鼠胸主动脉 ,将其置于 - 2 0℃冰浴中分别冷冻 1、2、4min ,观察血管内皮细胞冻结后的损伤情况 ,并探讨超氧化物歧化酶 (SOD)和维生素C对冻结所致血管损伤的保护作用。分别测定血管培养液中乳酸脱氢酶 (LDH)活力及血管中丙二醛 (MDA)水平。结果 血管暴露于 - 2 0℃环境 1、2、4min后 ,血管培养液中LDH活力分别较对照组升高 12 5 .6 %、15 6 .3%、184.2 % ,活力的增加与冷暴露时间呈正相关 (r =0 .932 ,P <0 .0 5 ) ;血管中MDA含量亦有不同幅度的增加 ,较对照组分别提高5 6 .5 3 %、6 2 .38%和 42 .99%。对冻结后的血管给予SOD(2 0 0U)或维生素C(12 .5mg)处理 ,可以明显降低血管MDA含量及培养液中LDH的活力。结论 脂质过氧化是冻结所致血管损伤的重要原因 ,SOD、维生素C可以通过清除自由基等抗氧化作用使冷冻对血管造成的损伤程度下降 。

Objective To observe the effects of free radicals on cold injured blood vessels and the corresponding therapeutic significance. Methods The aortic arteries were isolated from Wistar rats,followed by culturing in PBS medium for 30 min,and then exposed to -20 ℃ ice bath for 1,2,4 min,respectively.LDH activity and MDA level were measured.SOD and Vit C were used to protect the blood vessels from cold injury. Results LDH activity in the culture medium of vessels exposed to cold environment increased significantly by 125.6%,156.3%,184.2%,respectively.The degree of injury of blood vessels was time dependent.The level of MDA in the vessel homogenate increased by 56.53%,62.38%(P<0.05)and 42.99%(P>0.05) respectively.Treatment with SOD and Vit C could attenuate the production of MDA and LDH activity. Conclusion Lipid peroxidation may be the important cause in the injury of blood vessels exposed to cold.SOD and Vit C could attenuate the injury by antioxidation such as eliminating the free radicals.