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 malondialdehyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) were measured by biochemical method. The expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) were detected by enzyme linked immunosorbent 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 (PaCO(2)) and base excess (BE) were persistently decreased (P < 0.05 or P < 0.01). Oxygenation index (PaO(2)/FiO(2)) 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-alpha and IL-1 beta 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, PaO(2)/FiO(2), PaCO(2), 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.
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 malondialdehyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) were measured by biochemical method. The expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) were detected by enzyme linked immunosorbent 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 (PaCO(2)) and base excess (BE) were persistently decreased (P < 0.05 or P < 0.01). Oxygenation index (PaO(2)/FiO(2)) 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-alpha and IL-1 beta 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, PaO(2)/FiO(2), PaCO(2), 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.