Changes in tissue antioxidant enzyme activities and lipid peroxides in endotoxin-induced multiple organ failure.

Circulatory shock Pub Date : 1994-01-01
T Yoshikawa, H Takano, S Takahashi, H Ichikawa, M Kondo
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Abstract

Intravenous administration of bacterial endotoxin (lipopolysaccharide: LPS) induces shock and disseminated intravascular coagulation in rats. Our report here shows that LPS-administered rats (10 mg/100 g) develop tissue injuries and functional disorders in multiple vital organs. In the present study, we investigated changes in tissue antioxidant enzyme activities, neutrophil sequestration, and lipid peroxides in multiple organs (lung, stomach, small intestine for antioxidant enzyme activities and neutrophil sequestration; lung, stomach, small intestine, liver, abdominal aorta for lipid peroxides) of LPS-treated rats. LPS-treated animals morphologically revealed pulmonary interstitial edema, alveolar hemorrhage, and mucosal hemorrhage in the small intestine 45 min after LPS administration. Blood samples withdrawn from LPS-treated animals exhibited increases in serum amylase, blood urea nitrogen, creatinine, and transaminase levels up to 180 min post-LPS infusion. LPS-treated animals showed a significant increase in tissue myeloperoxidase (MPO) activities of the lung, but not of the small intestine and stomach 45 min after LPS infusion. Thiobarbituric acid reactive substances (TBARS) in the lung, small intestine, stomach, liver, and abdominal aorta significantly increased at 45 min post-LPS-infusion. Tissue superoxide dismutase (SOD) activities of the LPS-treated animals demonstrated a significant decrease in the lung, which suffered from severe insults and neutrophil sequestration; no significant change in the small intestine, which suffered from morphological insults without neutrophil sequestration, and a significant increase in the stomach, which showed no histological impairment, at 180 min post-LPS administration. Glutathione peroxidase (GSH-PX) activities of the lung and small intestine showed no significant change in LPS-treated rats, while those of the stomach revealed a marked increase.(ABSTRACT TRUNCATED AT 250 WORDS)

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内毒素诱导的多器官衰竭中组织抗氧化酶活性和脂质过氧化物的变化。
静脉注射细菌内毒素(脂多糖:LPS)可引起大鼠休克和弥散性血管内凝血。我们的报告显示,lps给药大鼠(10 mg/100 g)会出现组织损伤和多个重要器官的功能障碍。在本研究中,我们研究了组织抗氧化酶活性、中性粒细胞封存和脂质过氧化物在多器官(肺、胃、小肠)中抗氧化酶活性和中性粒细胞封存的变化;肺、胃、小肠、肝、腹主动脉(脂质过氧化物)。LPS处理动物在给药45 min后形态学显示肺间质水肿、肺泡出血和小肠黏膜出血。lps处理动物的血液样本显示,在lps输注后180分钟内,血清淀粉酶、血尿素氮、肌酐和转氨酶水平升高。LPS处理后45分钟,肺组织髓过氧化物酶(MPO)活性显著升高,小肠和胃组织髓过氧化物酶(MPO)活性无显著升高。lps输注后45 min,肺、小肠、胃、肝脏和腹主动脉的硫代巴比妥酸反应性物质(TBARS)显著升高。lps处理动物的肺组织超氧化物歧化酶(SOD)活性显著降低,肺组织受到严重损伤和中性粒细胞封存;lps给药180 min后,小肠无明显变化,无中性粒细胞隔离,小肠形态学损伤,胃无组织学损伤。lps处理大鼠肺和小肠的谷胱甘肽过氧化物酶(GSH-PX)活性无明显变化,而胃的GSH-PX活性明显升高。(摘要删节250字)
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