海水直接肺损伤的犬模型研究

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,PaCO2,pH,Ab,Be,潮气量，呼吸频率值与海水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程度支气管肺泡液充塞，其中LDH－L，ALP浓度持续显著升高（与对照和血液LDH－L，ALP浓度比较，P＜0．01），4h内海水未灌注区肺组织形态学结构无异常发现，结论：三组模型海水灌注区肺组织均发生损伤性改变，低氧血症和酸中毒的发生及其严重性与海水灌注区范围呈正相关。D组模型在排除了低氧血症和酸中毒等因素的作用后肺损伤明显，因此，海水淹溺后残留于肺内的海水可直接的导致严重的肺损伤，海水淹溺后是海水导致急性肺损伤的原发性因素。

Study of direct lung injury by seawater in canine models.

OBJECTIVE: To study the mechanism of direct lung injury by seawater and explore its possible management. METHODS: To exclude the interference of hypoxia and acidosis during the study of seawater-induced direct lung injury, 18 normal hybrid dogs were randomly assigned into group A (with all lung lobes perfused with seawater), group R (with the right lung lobe perfused with seawater) and group D (with the diaphragmatic lobe of lung perfused with seawater), with 6 dogs in each group. The changes in blood gas dynamics, blood gas acid-base status and electrolytes, along with the histological changes in the lung tissues were comparatively analyzed between the 3 groups. Bronchial microscope was employed to observe the continuous changes in the bronchioles before and after seawater perfusion in group D, and the concentration of the bronchoalveolar fluid and blood LDH-L and ALP levels were tested. RESULTS: The values of PaO(2), PaCO(2), pH, actual bicarbonate (AB), base excess (BE), tidal volume, and respiration rate in groups A and R were significantly different from those in group D (P < 0.01), and in groups A and R, the above measurements at every stage after seawater perfusion were significantly different from those before perfusion (P < 0.01). In group D, however, blood gas dynamics, blood gas acid-base status and electrolytes changed little after seawater perfusion (P > 0.05). In all the groups, obvious lung tissue injuries were observed under optical microscope after seawater perfusion. Observation with electron microscope revealed injuries to type II alveolar epithelial cells, broadened respiratory mucosa, and platelet adherence. Bronchial microscope in group D presented the bronchus filled with bronchoalveolar fluid, and blood LDH-L and ALP levels kept rising significantly (P < 0.01). Within 4 h after seawater perfusion, no pathological changes were seen in the lung tissues without direct contact with seawater. CONCLUSIONS: Seawater inspiration and retention in the lungs may lead to severe direct lung injury, and is the primary factor responsible for acute lung injury after drowning in the sea.