【摘要】 目的 觀察長期大量酒精攝入對大鼠心肌結構及心肌組織中丙二醛(MDA)、超氧化物歧化酶(SOD)和金屬硫蛋白(MT)含量的影響,探討氧化應激在酒精性心肌病大鼠中的作用。 方法 雄性健康SD大鼠45只,隨機分為2組,即對照組20只和模型組25只。模型組酒精濃度從5%、10%、20%和30%依次各自由飲1周,然后遞增至36%后以該濃度維持飼喂。對照組每日飲用與模型組酒精同等熱量的葡萄糖水。6個月后,觀察大鼠心肌組織的形態(tài)學改變及超微結構的變化,測定心肌組織中MDA、SOD及MT的含量。結果 模型組大鼠心肌細胞排列紊亂、間質充血、炎細胞浸潤、線粒體腫脹、空泡形成、肌絲溶解、核膜不規(guī)則和核仁裂解。心肌組織中MDA含量明顯升高(P lt;0.01),SOD活力含量明顯降低(P lt;0.01),MT含量明顯降低(P lt;0.01)。 結論 長期攝入大量酒精可使氧自由基代謝失衡,導致心肌損傷。氧化應激在酒精性心肌病發(fā)病機制中發(fā)揮著重要的作用。
【Abstract】 Objective To observe the effect of longterm and large quantities of alcohol intake on myocardial structure of rats and the content of malondialdehyde (MDA), superoxide dismutase (SOD) and metallothionein (MT) in myocardium tissue. To study the effect of oxidative stress on the rats with alcoholic cardiomyopathy. Methods Fortyfive male and healthy SD rats were randomly divided into the control group (20 rats) and model group (25 rats).The alcoholic concentrate in model group was increased from 5%,10%,20% to 30% every week, and maintain free drinking mass concentration of 36% alcohol. The control group drink the same calories of glucose water. Six months later, the myocardial tissues were observed both in light microscope and electron microscope .The level of MDA、SOD and MT were tested in myocardium tissue. Results In the model rats, the cells of myocardial disarray, interstitial congestion, inflammatory cell infiltration, mitochondrial swelling, vacuole formation, melt filaments, irregular nuclear membrane and nucleolus cracking. The content of MDA incresed(P lt;0.01)and the activities of SOD decreased(P lt;001),levels of MT decreased (P lt;0.01) in the cardiac muscular tissues in the model group compared with the control group. Conclusion Longterm intake of large amounts of alcohol can break the balance of oxygen free radicals, which leading to the damage of myocardial. Oxidative stress plays an important role in the etiopathogenesis of alcoholic cardiomyopathy.

引用本文： 程燕,孫堯,張浩良,關戰(zhàn)軍. 慢性大鼠酒精性心肌病氧化應激的影響. 華西醫(yī)學, 2010, 25(4): 660-. doi: 復制