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目的观察一氧化碳(CO)吸入对内毒素(LPS)诱导大鼠多器官(肺、肠)损伤的影响。方法18只SD大鼠随机均分为3组。损伤组静脉注入LPS 5 mg/kg体重,对照组注入生理盐水,CO吸入组在LPS诱导损伤后持续吸入CO。观察3 h后取回肠和肺叶,制作组织匀浆,离心后上清液。用酶联免疫吸附法(ELISA)测定肺肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6,肠血小板活化因子(PAF)、细胞间黏附分子(ICAM)-1水平；化学比色法测定丙二醛(MDA)含量、髓过氧化物酶(MPO)活性；光镜观察并盲法评分比较组织学变化；流式细胞仪检测细胞凋亡。结果LPS诱导损伤组肺TNF-α、IL-6、MDA、MPO及细胞凋亡分别增加3．15、2．37、6．10、1．36和26．50倍(P均＜0．05),肠PAF、ICAM-1、MDA、MPO及细胞凋亡分别增加2．42、2．05、4．43、2．10和5．17倍(P均＜0．05),器官损伤均较严重；CO吸入使损伤大鼠肺T NF-α、IL-6、MDA、MPO和凋亡指数分别下降39．5%、44．8%、19．7%、12．1%和81．1%(P均＜0．05),亦使肠PAF、ICAM-1、MDA、MPO和凋亡指数分别下降142．1%、105．6%、343．6%、110．4%和20．5%(P均＜0．05),器官损伤减轻。结论吸入一氧化碳通过拮抗过氧化损伤、减少促炎介质释放、抑制细胞凋亡而减轻LPS诱导的多器官损伤。
Objective To observe the effects of carbon monoxide (CO) inhalation on endotoxin (LPS) -induced injury of multiple organs (lung and intestine) in rats. Methods Eighteen SD rats were randomly divided into three groups. Rats in the injury group were given LPS 5 mg / kg body weight intravenously, saline was injected into the control group, and CO was inhaled continuously in CO inhalation group after LPS-induced injury. Observe the intestinal and lung lobes after 3 h, make tissue homogenate, and centrifuge the supernatant. The levels of tumor necrosis factor (TNF) -α, interleukin (IL) -6, intestinal platelet activating factor (PAF) and intercellular adhesion molecule (ICAM) -1 were measured by enzyme-linked immunosorbent assay The contents of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured by colorimetric method. Histopathological changes were observed by light microscopy and apoptosis was detected by flow cytometry. Results The levels of TNF-α, IL-6, MDA, MPO and apoptosis in LPS-induced injury group increased by 3.15, 2.37, 6.10, 1.36 and 26.50 times respectively ), Intestinal PAF, ICAM-1, MDA, MPO and apoptosis increased 2.42,2.05,4.43,2.10 and 5.17 times (all P <0.05) The levels of NF-|Á, IL-6, MDA, MPO and apoptosis index decreased by 39.5%, 44.8%, 19.7%, 12.1% and 81 in the lungs of rats with CO inhalation. (P <0.05), and also decreased the levels of PAF, ICAM-1, MDA, MPO and apoptosis index in the intestine by 142.1%, 105.6%, 343.6%, 110.4% and 20% .5% (all P <0.05), organ damage reduced. Conclusion Inhaled carbon monoxide attenuates LPS-induced multiple organ injury by antagonizing the effects of peroxisomes, decreasing the release of pro-inflammatory mediators and inhibiting apoptosis.