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目的:研究油酸致ARDS模型对疾病的长期模拟效果,并探讨内在机制。方法:选择健康新西兰大白兔30只,经左侧耳缘静脉按油酸0.1 ml/kg的剂量缓慢注入,观察动物呼吸、心率变化,测定氧合指数(PaO2/FiO2)、动脉氧分压、二氧化碳分压。分别于注射油酸后6小时、24小时、48小时以及72小时处死动物,收集静脉血及肺泡灌洗液(BALF),ELISA法检测肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)变化。H-E染色镜下观察肺部病理改变,计算肺组织含水量以判断肺损伤程度。结果:①所有模型动物在6小时内均出现ARDS表现。②6h组、24h组以及48h组氧合指数(PaO2/FiO2)与正常对照组相比均明显降低(P<0.05),且符合ARDS诊断标准。72h组氧合指数(PaO2/FiO2)虽然也明显降低,但未达到ARDS的诊断标准。③血浆中TNF-α与IL-6明显升高(P<0.05),于致伤后72小时后有所恢复,但仍高于正常。BALF中TNF-α也出现相同变化趋势,而IL-6则在试验期间持续高表达。④镜下可见两肺充血、出血,肺泡及肺间质水肿,透明膜形成,大量中性粒细胞浸润,终末支气管上皮细胞变性坏死,双肺含水量明显增加(p<0.05)。结论:兔静脉注射油酸48小时内可以稳定模拟ARDS病理生理状态和临床表现,72小时后该模型部分指标恢复,很可能与中性粒细胞活性降低以及兔本身代偿有关。
OBJECTIVE: To study the long-term simulation effect of oleic acid-induced ARDS model on the disease and to explore the underlying mechanism. Methods: Thirty healthy New Zealand white rabbits were injected slowly with 0.1 ml / kg oleic acid via the left ear veins. The respiration and heart rate of the animals were observed. The PaO2 / FiO2, Carbon dioxide partial pressure. Animals were sacrificed at 6 hours, 24 hours, 48 hours and 72 hours after injection of oleic acid, respectively. Venous and BALF were collected and the levels of tumor necrosis factor alpha (TNF-α), interleukin 6 IL-6) changes. H-E staining under the microscope pathological changes in the lungs to calculate the water content to determine the degree of lung injury. Results: ① ARDS appeared in all model animals within 6 hours. ② The oxygenation index (PaO2 / FiO2) of 6h group, 24h group and 48h group were significantly lower than those of the normal control group (P <0.05), and they were consistent with the ARDS diagnostic criteria. 72h group oxygenation index (PaO2 / FiO2) although significantly reduced, but did not meet the diagnostic criteria of ARDS. ③ The levels of TNF-α and IL-6 in plasma were significantly increased (P <0.05), and recovered after 72 hours of injury but still higher than normal. The same tendency was observed in TNF-α in BALF, while IL-6 was consistently high in the experiment. (4) The lungs showed congestion, hemorrhage, alveolar and pulmonary interstitial edema, transparent membrane formation, massive neutrophil infiltration, terminal degeneration and necrosis of bronchial epithelial cells, lung water content increased significantly (p <0.05). Conclusion: Intravenous injection of oleic acid can stably simulate the pathophysiology and clinical manifestations of ARDS within 48 hours. After 72 hours, some indicators of the model recover, which may be related to the decrease of neutrophil activity and the compensation of rabbits themselves.