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暴露于高氧、低氧和缺血影响下的大鼠肺部的脂质过氧化作用。

Lipid peroxidation in lung of rats exposed to hyperoxic, hypoxic and ischemic effects.

作者信息

Török B, Röth E, Zsoldos T, Tigyi A, Matkovics B, Szabó L

出版信息

Exp Pathol. 1986;29(4):221-6. doi: 10.1016/s0232-1513(86)80026-3.

Abstract

Rat experiments were undertaken to describe the range of the endogenous lipid peroxidation (measured by formation of malondialdehyde [MDA] in lung tissue) and to analyze the effects of hyperoxic, hypoxic and ischemic influences. The acute hyperoxia caused a moderate increase in lipid peroxidation. The MDA formation in lungs of rats was perceptibly higher in low oxygen environment, while the highest values were found in ischemic lungs. The cytotoxic metabolites cause unfavourable influences on the lung structure (perivascular, interstitial and alveolar edema, destroyed epithelial lining with disintegration of lamellar membranes of the type II-pneumocytes). The findings suggest that potential danger of the oxygen free radicals is an increased lipid peroxidation of lung tissue causing alveolocapillary destruction and extensive exudation with pathologic dwindling of lung function.

摘要

进行大鼠实验以描述内源性脂质过氧化的范围(通过肺组织中丙二醛[MDA]的形成来衡量),并分析高氧、低氧和缺血影响的作用。急性高氧导致脂质过氧化适度增加。在低氧环境中,大鼠肺中的MDA形成明显更高,而在缺血肺中发现的值最高。细胞毒性代谢产物对肺结构产生不利影响(血管周围、间质和肺泡水肿,II型肺细胞板层膜解体导致上皮衬里破坏)。研究结果表明,氧自由基的潜在危险是肺组织脂质过氧化增加,导致肺泡毛细血管破坏和广泛渗出,肺功能病理性下降。

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