Kumar K V, Rao S M, Gayani R, Mohan I K, Naidu M U
Central Research Laboratory, Departments of Clinical Pharmacology and Therapeutics, Nizam' Institute of Medical Sciences, Hyderabad, India.
Clin Chim Acta. 2000 Aug;298(1-2):111-20. doi: 10.1016/s0009-8981(00)00264-3.
Oxygen free radicals are important mediators of both physiological and pathological events. In acute lung injury, the activated lymphocytes stimulate tumor necrosis factor (TNF) and other cytokines. These lymphokines augment free radical generation by polymorphonuclear leukocytes (PMNLs), macrophages and other cells which may ultimately produce acute respiratory distress syndrome (ARDS). This is supported by our results presented here in that there is a significant increase in lipid peroxidation products in patients with established ARDS. The amount of lipid peroxidation was significantly higher in the established ARDS group compared to patients who are at risk for ARDS. Nitric oxide concentrations were significantly decreased in established ARDS compared to the control and those who are at risk for ARDS. Fatty acid analysis of the plasma phospholipid fraction revealed a significant decreased in linoleic acid, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid levels of n-6 series and alpha-linolenic acid, eicosapentaenoic acid, docosa-hexanenoic acid of n-3 series. Patients who are at risk for ARDS have decreased levels of gamma-linolenic acid of the n-6 series, alpha-linolenic acid and eicosapentaenoic acid of the n-3 series. These results suggest that lipid peroxides and alteration in essential fatty acid metabolism may have a role in the pathogenesis of ARDS.
氧自由基是生理和病理过程的重要介质。在急性肺损伤中,活化的淋巴细胞刺激肿瘤坏死因子(TNF)和其他细胞因子。这些淋巴因子会增加多形核白细胞(PMNLs)、巨噬细胞和其他细胞产生的自由基,最终可能导致急性呼吸窘迫综合征(ARDS)。我们在此展示的结果支持了这一点,即确诊为ARDS的患者脂质过氧化产物显著增加。与有ARDS风险的患者相比,确诊ARDS组的脂质过氧化量显著更高。与对照组和有ARDS风险的患者相比,确诊ARDS患者的一氧化氮浓度显著降低。血浆磷脂部分的脂肪酸分析显示,n-6系列的亚油酸、γ-亚麻酸、二高-γ-亚麻酸和花生四烯酸水平以及n-3系列的α-亚麻酸、二十碳五烯酸、二十二碳六烯酸水平显著降低。有ARDS风险的患者n-6系列的γ-亚麻酸、n-3系列的α-亚麻酸和二十碳五烯酸水平降低。这些结果表明,脂质过氧化物和必需脂肪酸代谢改变可能在ARDS的发病机制中起作用。