Pulmonary changes in a mouse model of combined burn and smoke inhalation-induced injury
Pulmonary changes in a mouse model of combined burn and smoke inhalation-induced injury
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DOI：
10.1152/japplphysiol.00232.2007
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发表时间：
2008-08-01
影响因子：
3.3
通讯作者：
Traber, Daniel L.
中科院分区：
文献类型：
--
作者：
Mizutani, Akio;Enkhbaatar, Perenlei;Traber, Daniel L.
当烧伤合并烟雾吸入时，烧伤患者的发病率和死亡率增加。本研究的目的是建立烧伤和烟雾吸入性损伤的小鼠模型，以更准确地揭示这些病理变化的机制方面。烧伤小鼠组仅接受40%总体表面积的三度烧伤，烟雾吸入性损伤小鼠组仅接受两次30 s的棉花烟雾暴露，而烧伤和烟雾吸入性损伤联合小鼠组同时接受烧伤和烟雾吸入性损伤。监测动物存活120 h。烧伤组、烟雾吸入性损伤组和复合伤组的存活率分别为70%、60%和30%。接受烧伤和烟雾联合损伤的小鼠发生了更大的肺损伤，这可以通过组织学变化（间隔增厚和间质水肿）和更高的肺含水量来证明。这些小鼠还表现出更严重的肺气体交换受损[动脉Po-2（Pa-O2）/吸入O-2分数（F-IO 2）< 200]。肺髓过氧化物酶活性显着高于烧伤和烟雾损伤的动物与其他三个实验组相比。血浆NO2-/NO3-、肺诱导型一氧化氮合酶（iNOS）活性和iNOS mRNA随损伤增加而增加;然而，烧伤和烟雾损伤组表现出更高的反应。烧伤和烟雾吸入性损伤的严重程度与肺组织中一氧化氮的产生和活化白细胞的积累有关。烧伤和烟雾吸入性损伤的小鼠模型使我们能够更好地了解继发于烧伤和烟雾吸入性损伤的心肺疾病的病理生理机制。
The morbidity and mortality of burn victims increase when burn injury is combined with smoke inhalation. The goal of the present study was to develop a murine model of burn and smoke inhalation injury to more precisely reveal the mechanistic aspects of these pathological changes. The burn injury mouse group received a 40% total body surface area third-degree burn alone, the smoke inhalation injury mouse group received two 30-s exposures of cotton smoke alone, and the combined burn and smoke inhalation injury mouse group received both the burn and the smoke inhalation injury. Animal survival was monitored for 120 h. Survival rates in the burn injury group, the smoke inhalation injury group, and the combined injury group were 70%, 60%, and 30%, respectively. Mice that received combined burn and smoke injury developed greater lung damage as evidenced by histological changes (septal thickening and interstitial edema) and higher lung water content. These mice also displayed more severely impaired pulmonary gas exchange [arterial Po-2 (Pa-O2)/inspired O-2 fraction (F-IO2) < 200]. Lung myeloperoxidase activity was significantly higher in burn and smoke-injured animals compared with the other three experimental groups. Plasma NO2-/NO3-, lung inducible nitric oxide synthase (iNOS) activity, and iNOS mRNA increased with injury; however, the burn and smoke injury group exhibited a higher response. Severity of burn and smoke inhalation injury was associated with more pronounced production of nitric oxide and accumulation of activated leukocytes in lung tissue. The murine model of burn and smoke inhalation injury allows us to better understand pathophysiological mechanisms underlying cardiopulmonary morbidity secondary to burn and smoke inhalation injury.