Pathophysiologic events related to thermal injury of skin.
Pathophysiologic events related to thermal injury of skin.
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DOI：
10.1097/00005373-199012001-00018
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发表时间：
1990-12
期刊：
影响因子：
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通讯作者：
Peter A. Ward;G. Till
中科院分区：
文献类型：
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作者：
Peter A. Ward;G. Till
皮肤急性热损伤相当于二级损伤，约占全身表面积的25%，导致一系列病理生理事件，导致局部和远端组织/器官损伤。远端效应涉及血管内溶血和急性肺损伤，这两者都可归因于补体激活和中性粒细胞的血管内刺激，导致氧自由基产生，从而导致红细胞和肺血管内皮细胞损伤。在热损伤的局部部位，血管通透性的进行性增加与补体激活和组胺释放有关，其结果是组胺与黄嘌呤氧化酶的相互作用，导致酶的催化活性增强。黄嘌呤氧化酶的有毒氧产物，包括H2 O2及其转化产物羟基自由基，似乎与真皮血管内皮细胞的损伤有关，导致进行性血管渗透性。使用黄嘌呤氧化酶抑制剂、组胺释放抑制剂（色甘酸）、过氧化氢酶、铁螯合剂（去铁胺）或羟基自由基清除剂可以大大减弱血管渗透性的增加。有趣的是，中性粒细胞似乎在热创伤动物模型中的真皮血管损伤中几乎没有发挥任何作用。这些研究表明，局部热创伤后的病理生理事件是复杂的，涉及多种介质途径。
Acute thermal injury of skin equivalent to second-degree injury and involving approximately 25% of total body surface results in a series of pathophysiologic events which lead to both local and distant tissue/organ injury. The distant effects involve intravascular hemolysis and acute lung injury, both of which can be attributed to complement activation and intravascular stimulation of neutrophils, resulting in oxygen radical production, which results in injury of red cells and pulmonary vascular endothelial cells. At the local site of thermal injury, the progressive increase in vascular permeability is linked to complement activation and histamine release, the outcome of which is interaction of histamine with xanthine oxidase, resulting in enhanced catalytic activity of the enzyme. Toxic oxygen products of xanthine oxidase, including H2O2 and its conversion product, the hydroxyl radical, appear to be linked to the damage of dermal vascular endothelial cells, resulting in progressive vascular permeability. The increased vascular permeability can be greatly attenuated by the use of inhibitors of xanthine oxidase, the inhibitor of histamine release (cromolyn), catalase, an iron chelator (deferoxamine), or scavengers of the hydroxyl radical. Interestingly, neutrophils appear to play little if any role in dermal vascular injury in this animal model of thermal trauma. Those studies suggest that pathophysiologic events following local thermal trauma are complex and involve a variety of mediator pathways.