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目的建立海水直接肺损伤的犬模型,为研究海水及其成分对肺直接损伤机制及其治疗提供研究平台。方法排除低氧血症和酸中毒等因素对海水直接肺损伤的影响,选择18只健康犬随机分为3组(n=6), 即全肺海水灌注组( A组)、右肺海水灌注组( R组)和右膈叶海水灌注组即海水直接肺损伤组(D组)。对比观察三组血流动力学、血气酸碱、电解质等指标以及肺组织细胞学改变,以支气管纤维镜连续观察D组三级支气管内海水灌注前后的变化,检测支气管肺泡液和血液乳酸脱氢酶(LDH-L)、碱性磷酸酶(ALP)浓度。结果(1)D组的动脉氧分压(PaO2)、动脉二氧化碳分压(PaCO2)、pH、实际重碳酸盐(AB)、过剩碱(BE)、呼吸频率、潮气量值与其余两组比较有显著差异(P<0.01)。(2)A组和R组各时段PaO2、Pa-CO2、pH、AB、BE、潮气量、呼吸频率值与海水灌注前相比有显著差异(P<0.01)。(3)D组血流动力学和血气酸碱及电解质等指标与海水灌注前相比无统计学差异(P>0.05)。(4)三组海水灌注区肺组织损伤均明显,出现充血水肿,局部有暗红色片状改变和梗死出血灶,光镜下可见肺泡水肿、肺泡萎陷、肺间质充血水肿明显及大量中性粒细胞浸润和肺出血。电镜下可见肺泡Ⅱ型上皮细胞损伤、呼吸膜增宽、血小板附壁。(5)支气管纤维镜连续观察D组海水灌注区支气管有不同?
Objective To establish a canine model of direct lung injury in seawater and provide a research platform for studying the mechanism and treatment of direct lung injury caused by seawater and its components. Methods Excluding the effects of hypoxemia and acidosis on the direct lung injury in seawater, 18 healthy dogs were randomly divided into 3 groups (n = 6), ie, whole lung seawater perfusion group (group A), right lung seawater perfusion Group (R group) and right diaphragmatic seawater perfusion group that seawater direct lung injury group (D group). The changes of hemodynamics, acidity and alkalis, electrolytes and cytology in lung tissue of the three groups were observed and compared. The level of bronchial alveolar fluid and blood lactate dehydrogenation Enzyme (LDH-L), alkaline phosphatase (ALP) concentration. Results (1) PaO2, PaCO2, pH, actual bicarbonate (AB), excess base (BE), respiration rate and tidal volume in group D were compared with the other two groups There was significant difference (P <0.01). (2) PaO2, Pa-CO2, pH, AB, BE, tidal volume and respiratory rate in group A and group R were significantly different from those before seawater perfusion (P <0.01). (3) There was no significant difference in hemodynamics and acid, alkali and electrolytes between group D and before water perfusion (P> 0.05). (4) Three groups of seawater perfusion area lung tissue injury were obvious congestion and edema, local dark red flake changes and infarct hemorrhage, light microscopy showed alveolar edema, alveolar collapse, pulmonary interstitial congestion and edema and a lot of Granulocyte infiltration and pulmonary hemorrhage. Electron microscopy showed alveolar type Ⅱ epithelial cell injury, respiratory membrane widening, platelet adhesion. (5) bronchial fiberoscope continuous observation of the group D seawater perfusion bronchus have different?