Effect of N-acetylcysteine on pulmonary damage due to microembolism in the rat.

T Wegener, B Sandhagen, T Saldeen
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Abstract

The effect of N-acetylcysteine (NAC), a free radical scavenger, was investigated in a microembolism rat model of adult respiratory distress syndrome (ARDS). Microembolism was induced by an intravenous injection of bovine thrombin and an intraperitoneal injection of a fibrinolysis inhibitor, trans-4-aminomethyl-cyclohexane-carboxylic acid (AMCA). NAC counteracted the experimentally induced increase in lung weight, the development of alveolar oedema, and the amount of fibrin in precapillary vessels. There was also a tendency to a decrease of the experimentally induced interstitial oedema caused by the NAC treatment, although it was not statistically significant. Surprisingly, NAC reduced plasma viscosity in both experimental and control animals. It also seemed to increase PaO2 in animals with pulmonary damage, but had a lowering effect on PaO2 in control animals. The results indicate that NAC has a significant preventive effect in this microembolism rat model of ARDS, and that this effect may be achieved through decreased deposition of fibrin, thus counteracting pulmonary oedema, and a decrease in plasma viscosity.

n -乙酰半胱氨酸对大鼠微栓塞所致肺损伤的影响。
研究了自由基清除剂n -乙酰半胱氨酸(NAC)在成人呼吸窘迫综合征(ARDS)微栓塞大鼠模型中的作用。微栓塞是通过静脉注射牛凝血酶和腹腔注射纤维蛋白溶解抑制剂反式4-氨基甲基环己烷-羧酸(AMCA)诱导的。NAC抵消了实验诱导的肺重量增加、肺泡水肿的发展和毛细血管前纤维蛋白的数量。NAC治疗引起的实验性间质性水肿也有减少的趋势,但无统计学意义。令人惊讶的是,NAC降低了实验动物和对照动物的血浆粘度。它似乎也增加了肺损伤动物的PaO2,但对对照组动物的PaO2有降低作用。结果表明,NAC在ARDS微栓塞大鼠模型中具有显著的预防作用,其作用机制可能是通过减少纤维蛋白沉积,从而抵消肺水肿,降低血浆粘度。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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