| Objective: To investigate the pathophysiologic change of traumatic brain edema (TBE) accompanied with the pulmonary edema after seawater drowning (PE-SWD),to observe the effect and the mechanism of ulinastatin on TBE accompanied with PE-SWD.Methods: Establish an animal model of moderate brain trauma with pulmonary edema after seawater drowning in rat. (1) At 1h, 6h, 12h, 24h and 48h postinjury, blood gas analysis was performed, the water contents of the brain and lung were measured, the concentration of interleukin 1β(IL-1β) and tumor necrosis factorα(TNF-α) in the serum, brain homogenates and lung homogenates were determined and histopathology changes of brain and lung at 24h postinjury were observed. (2) 24 hours after intraperitoneal injection of ulinastatin, the change of water contents and the concentration of IL-1βand TNF-αwere measured and histopathology changes of brain and lung were observed.Results: Significant hypoxemia and acidosis were observed associated with the seawater drowning. Compared with the TBI alone, the seawater alone or the TBI with freshwater, the cerebral water contents of rats in the TBI with seawater drowning group increased significantly. The concentration of IL-1βand TNF-αin the serum, brain and lung also changed. Both the water contents and the concentration of IL-1βand TNF-αwere markedly decreased by the intervention of ulinastatin.Conclusion: Our results indicate that hypoxemia and acidosis are the main pathophysiologic mechanism of the development of PE-SWD and its exacerbation effect on the TBE. Seawater is an important detrimental factor. Inflammatory response may play an important role in both TBE and PE-SWD. Administration of ulinastatin may be considered a potential therapeutic agent in TBE accompanied with PE-SWD.
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