海水和淡水淹溺致肺损伤的比较

目的 比较海水和淡水淹溺动物造成肺损伤作用的差异.方法 42只新西兰兔随机分成对照组(n=18)、淡水组(n=12)和海水组(n=12).经气管插管灌注2 ml/kg淡水或海水制备淹溺动物模型.连续监测血压、心率(HR)、呼吸、血气分析、电解质等指标变化;计算肺湿/干重(W/D)比值、肺通透指数(LPI);检测肺组织髓过氧化物酶(MPO)、丙二醛(MDA)和超氧化物歧化酶(SOD)活性;用酶联免疫吸附法(ELISA)分析肺组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)表达水平;同时进行病理学检查,并计算肺损伤评分.结果 3组间电解质、HR差异无统计学意义(P均>0.05).淡水组呼吸频率(RR)迅速升高(P<0.05),氧合指数(PaO2/FiO2)0.5 h略低于300 mm Hg(1 mm Hg=0.133 kPa),此后迅速升至300 mm Hg以上,并于2 h接近起点水平;血气分析显示pH值虽无差异,但动脉血二氧化碳分压(PaCO2)、剩余碱(BE)持续低于起点(P<0.05或P<0.01);平均动脉压(MAP)仅于5 min呈一过性升高;肺大体标本局部可见淤血灶,显微镜下以肺泡塌陷,微血管充血为主;肺W/D比值、LPI无明显变化,肺损伤评分显著高于对照组(P均<0.01);肺组织MPO、MDA、TNF-α和IL-1β的升高及SOD的降低差异具有统计学意义(P<0.05或P<0.01).海水组动物症状比淡水组重,肉眼可见肺充血、水肿严重,体积明显增大,重力依赖区呈暗红色肝样变,显微镜下以炎细胞浸润和肺泡水肿为主;W/D比值、LPI明显升高(P均<0.01),RR、MAP、PaO2/FiO2、PaCO2、BE及肺组织炎症介质升高或降低的程度均比淡水组显著而持久,海水6 h组肺损伤评分也显著高于淡水组及海水3 h组(P<0.05或P<0.01).结论 海水或淡水淹溺不仅会直接损伤肺实质细胞,还会激活急性炎症反应;海水淹溺引起的肺损伤比淡水严重.

Differences between seawater- and freshwater-induced lung injuries

Objective To investigate the differences between the lung injuries induced by seawater and freshwater drowning in a rabbit model. Methods Forty-two New Zealand rabbits were divided randomly into three groups: control group (C, n=18), freshwater drowning group (F, n=12), seawater drowning group (S, n=12). The drowning model was established by pouring seawater or freshwater (2 ml/kg) into the respiratory tract through a tracheal catheter. Mean arterial pressure (MAP) and heart rate (HR) were monitored continually. Respiratory rate (RR), blood gas analysis and electrolyte contents of every rabbit were observed at different time. The lung wet to dry weight (W/D) ratio and lung permeability index (LPI) were calculated. The contents of malondialdenyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) were measured by biochemical method. The expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by enzyme linked immunosorbeut assay (ELISA). At the same time, the changes in pathology were studied with by hematoxylin eosin (HE) staining, and lung pathologic score (LPS) was calculated. Results There was no significant difference in blood electrolyte contents and HR among the three groups (all P>0.05). In freshwater drowning, there was a temporary increase of MAP at 5 minutes, RR increased immediately, and partial pressure of carbon dioxide in artery (PaCO2) and base excess (BE) were persistently decreased (P<0.05 or P<0.01). Oxygenation index (PaO2/FiO2) fell to (297.8±81.3) mm Hg (1 mm Hg=0.133 kPa) at 0.5 hour, then elevated to over 300 mm Hg rapidly, and then reverted to initiative level in around 2 hours. There were several edematous and petechial areas on the dependent region of the lung. Alveolar collapse and parenchymal congestion were the main pathological features. W/D ratio and LPI showed no remarkable change. In lung tissue, the level of LPS, MPO, MDA, TNF-α and IL-1β had a significant increase, while SOD had a significant decrease (P<0.05 or P<0.01). In S group, respiratory symptoms were more serious;edematous and congestive areas of the lung were more extensive, and the dependent region showed hepatization changes. W/D ratio and LPI consisted of elevated significantly (all P<0.01). The pathological characteristics were massive inflammatory cell infiltration and more serious alveolar edema. Compared with F group, the extent of up- or down-regulation of RR, MAP, PaO2/FiO2, PaCO2, BE, inflammatory media and cytokines in S group was more prominent and steady, and S 6-hour group had a higher pathological score than S 3-hour group and F group (P<0.05 or P<0.01). Conclusion Seawater and freshwater drowning could not only injure pulmonary parenchymal cells directly, but also induce acute inflammatory reaction. Lung injury induced by seawater is severer than that by freshwater.