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目的了解高密度脂蛋白(HDL)对严重烫伤大鼠肺功能的作用及其机制。方法将Wistar大鼠分为对照组(15只)、烫伤组(60只)和HDL组(60只)。对照组大鼠不作处理;其余2组均造成30%TBSAⅢ度烫伤,伤后常规补液,其中HDL组伤后立即经尾静脉注入HDL(80 mg/kg)。检测2组烫伤大鼠伤后12、24、48、72 h血清胞间黏附分子1(ICAM-1)及肿瘤坏死因子α(TNF-α)的含量,并检测其动脉血二氧化碳分压(PCO_2)、氧分压(PO_2);观察大鼠伤后各时相点肺组织病理学变化。另检测对照组上述指标。结果与对照组比较,烫伤组大鼠伤后各时相点ICAM-1、TNF-α的含量及PCO_2均显著升高(P<0.05或P<0.01),PO_2显著降低(P<0.05)。HDL组上述指标与对照组比较,差异无统计学意义(P>0.05);但与烫伤组比较,各时相点ICAM-1、TNF-α含量均显著降低(P<0.05或P<0.01)。伤后48 h,烫伤组ICAM-1、TNF-α分别为(3.42±0.25)μg/L、(4.04±0.28)ng/L,明显高于HDL组[(2.24±0.14)μg/L、(3.35±0.22)ng/L,P<0.05或P<0.01]。烫伤组大鼠伤后48 h肺小血管周围炎性细胞浸润,肺内血管扩张出血,部分小血管管腔内红细胞淤滞凝集,形成“假血栓”;肺毛细血管内皮细胞连接松弛,内皮细胞水肿。HDL组肺内小血管周围炎性细胞浸润明显减轻;肺毛细血管内皮细胞连接较紧密。结论HDL对严重烫伤大鼠肺功能具有保护作用,可能与其抑制ICAM-1、TNF-α表达有关。
Objective To investigate the effect of high density lipoprotein (HDL) on lung function in severely scalded rats and its mechanism. Methods Wistar rats were divided into control group (n = 15), burn group (n = 60) and HDL group (n = 60). The control group rats were not treated; the remaining two groups were caused by 30% TBSA Ⅲ degree scald, conventional fluid rehydration, HDL group immediately after the injection of HDL (80 mg / kg) through the tail vein. The contents of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α) were detected at 12, 24, 48 and 72 h after injury in two groups of scalded rats and their arterial partial pressure of carbon dioxide ) And partial pressure of oxygen (PO_2). Pathological changes of lung tissue were observed at different time points after injury. Another test control group of the above indicators. Results Compared with the control group, the levels of ICAM-1, TNF-α and PCO 2 were significantly increased (P <0.05 or P <0.01) and PO 2 significantly decreased in scalded rats at each time point after injury (P <0.05). Compared with the scald group, the levels of ICAM-1 and TNF-αin the HDL group were significantly lower than those in the control group (P <0.05 or P <0.01) . The levels of ICAM-1 and TNF-α in scalded group were (3.42 ± 0.25) μg / L and (4.04 ± 0.28) ng / L respectively at 48 h after injury, which were significantly higher than those in HDL group [(2.24 ± 0.14) μg / 3.35 ± 0.22) ng / L, P <0.05 or P <0.01]. At 48 hours after injury in scalded rats, inflammatory cell infiltration around the small pulmonary vessels, vasodilation and bleeding in the lungs, agglutination of red blood cell stasis in some small blood vessels and formation of “false thrombosis”; relaxation of pulmonary capillary endothelial cells, Cell edema. In the HDL group, the infiltration of inflammatory cells in the small blood vessels around the lung was significantly reduced; the pulmonary capillary endothelial cells were more closely connected. Conclusion HDL may have a protective effect on lung function in severely scalded rats, which may be related to the inhibition of ICAM-1 and TNF-α expression.