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胸部开放伤后胸腔海水浸泡对犬血管内皮细胞功能的影响
引用本文:薛志强,段蕴铀,孟激光,胡晓红,丁新民,彭朝胜. 胸部开放伤后胸腔海水浸泡对犬血管内皮细胞功能的影响[J]. 中华航海医学与高气压医学杂志, 2009, 17(5): 81-84. DOI: 10.3760/cma.j.issn.1009-6906.2010.02.006
作者姓名:薛志强  段蕴铀  孟激光  胡晓红  丁新民  彭朝胜
作者单位:解放军总医院胸外科,北京,100853;海军总医院呼吸科;
摘    要:目的 探讨胸部开放伤后胸腔海水浸泡对犬血管内皮细胞功能的影响.方法 12只健康成年杂交犬随机分为单纯开放性气胸组(A组)和胸腔海水浸泡组(B组).检测犬致伤后动脉血气、血电解质、渗透压变化以及血管内皮细胞标记物循环内皮细胞(CEC)、血管性假性血友病因子(vWF)、血栓素(TXB_2)、前列腺素(PGF_(1a))、内皮素(ET)的变化.结果 A组犬致伤后1h动脉血氧分压(PaO_2)最低,然后逐渐恢复,B组犬致伤后PaO_2进行性下降,伤后6 haO_2/吸入气体中氧气的百分含量(FiO_2)<300,达到急性肺损伤(ALI)诊断标准,并伴有高钠、高氯、高渗透压血症.B组外周血CEC记数、vWF、TXB_2、ET在伤后4、6 h较伤前显著升高(P<0.05).B组犬外周血TXB_2、ET伤后4、6显著高于A组(P<0.05),PGF_(1a)与A组差异无统计学意义(P>0.05).结论 胸部开放伤后胸腔海水浸泡引起大量血管活性物质释放及血管内皮细胞损伤,参与了ALI的发生.

关 键 词:海水浸泡   急性肺损伤   血管内皮细胞   胸部开放伤   

Effects of thoracic cavity seawater immersion on vascular endothelial cells following open chest injury in dogs
XUE Zhi-qiang,DUAN Yun-you,MENG Ji-guang,HU Xiao-hong,DING Xin-min,PENG Chao-sheng. Effects of thoracic cavity seawater immersion on vascular endothelial cells following open chest injury in dogs[J]. Chinese Journal of Nautical Medicine and Hyperbaric Medicine, 2009, 17(5): 81-84. DOI: 10.3760/cma.j.issn.1009-6906.2010.02.006
Authors:XUE Zhi-qiang  DUAN Yun-you  MENG Ji-guang  HU Xiao-hong  DING Xin-min  PENG Chao-sheng
Abstract:Objective To investigate effects of thoracic cavity seawater immersion on vascular endothelial cells following open chest injury in dogs. Methods Twelve healthy hybrid dogs were randomly divided into 2 groups: group A, animals with open chest injury; group B, animals with thoracic cavity seawater immersion following open chest injury. Arterial gas analysis, plasma osmotic pressure and serum electrolytes were measured at different time points. Blood samples were collected to measure circulating endothelial cells (CEC), von Willebrand Factor (vWF), TXB_2, PGF_(1a), and endothelin (ET). Results Arterial oxygen partial pressure (PaO_2) and oxygenation indices for the animals of group A and group B decreased markedly after injury, then recovered gradually, while arterial oxygen partial pressure (PaO_2) for the animals of group B decreased progressively and oxygenation indices (PaO_2/FiO_2) were lower than 300 at hour 6 following injury, conforming with the diagnostic standards of acute lung injury (ALI) and high elevations were noted in Na~+, K~+, and hyperosmotic pressure. CEC and the concentrations of vWF, TXB_2 and ET increased significantly for animals in group B at hour 4 and 6 after injury, when compared with those before injury (P < 0.05). TXB_2 and ET at hour 4 and 6 after injury for the animals of group B were significantly higher than those of the animals of group A(P <0.05). No statistical differences could be seen in PGF_(1a), when compared with that of group A (P >0.05). Conclusions Thoracic cavity seawater immersion after open chest injury could activate the release of many vaso-active substances, induce lesion of vascular endothelial ceils, which might be involved in acute lung injury.
Keywords:Seawater immersionAcute lung injuryVascular endothelial cellOpen chestinjury
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