通過犬膽道梗阻模型,動態(tài)觀察了膽道梗阻后不同時相肝組織內(nèi)超氧化物歧化酶(SOD)及丙二醛(MDA)含量變化。結(jié)果發(fā)現(xiàn):犬膽道梗阻后2周其肝組織MDA含量較對照組明顯升高(P<0.01),梗阻后3周SOD含量亦有顯著下降(P<0.05),且二者變化隨著梗阻時間的延長而加重。表明膽道梗阻后肝臟對自由基的清除能力下降,脂質(zhì)過氧化反應(yīng)增強,可能是膽道梗阻導(dǎo)致肝損傷的原因之一。
引用本文: 李靖,遲彥邦,方學(xué)軍. 犬膽道梗阻后肝臟超氧化物歧化酶及過氧化脂質(zhì)的變化. 中國普外基礎(chǔ)與臨床雜志, 1998, 5(3): 148-149. doi: 復(fù)制
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- 2. 遲彥邦,黃志強,張建超等. 實驗性膽道阻塞性黃膽對肝、腎、肺的損害. 重慶醫(yī)藥, 1983; 11(6)∶53.
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- 4. Tsai LY, Lee KT, Tsai SM, et al. Changes of lipid peroxide levels in blood and liver tissue of patients with obstructive jaundice. Chinica Chimica Acta, 1993; 215(1)∶41.
- 5. 程迅生,遲彥邦,祁佐元. 慢性膽道梗阻時肝臟血流量及微血管床的變化. 中華外科雜志, 1992;30 (12)∶ 751.
- 6. Parks DA. Oxygen radicals∶mediators of gastrointestinal pathophysiology. Gut, 1989; 30(3)∶293.
- 7. Slater IF. Free radical mechanisms in tissue injury. Biochem J, 1984; 222(1)∶1.