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联合辐射与烧伤损伤模型的建立。

Development of a combined radiation and burn injury model.

作者信息

Palmer Jessica L, Deburghgraeve Cory R, Bird Melanie D, Hauer-Jensen Martin, Kovacs Elizabeth J

机构信息

Department of Surgery, Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, Illinois, USA.

出版信息

J Burn Care Res. 2011 Mar-Apr;32(2):317-23. doi: 10.1097/BCR.0b013e31820aafa9.

DOI:10.1097/BCR.0b013e31820aafa9
PMID:21233728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3062624/
Abstract

Combined radiation and burn injuries are likely to occur after nuclear events, such as a meltdown accident at a nuclear energy plant or a nuclear attack. Little is known about the mechanisms by which combined injuries result in higher mortality than by either insult alone, and few animal models exist for combined radiation and burn injury. Herein, the authors developed a murine model of radiation and scald burn injury. Mice were given a single dose of 0, 2, 4, 5, 6, or 9 Gray (Gy) alone, followed by a 15% TBSA scald burn. All mice receiving ≤4 Gy of radiation with burn survived combined injury. Higher doses of radiation (5, 6, and 9 Gy) followed by scald injury had a dose-dependent increase in mortality (34, 67, and 100%, respectively). Five Gy was determined to be the ideal dose to use in conjunction with burn injury for this model. There was a decrease in circulating white blood cells in burn, irradiated, and combined injury (5 Gy and burn) mice by 48 hours postinjury compared with sham (49.7, 11.6, and 57.3%, respectively). Circulating interleukin-6 and tumor necrosis factor-α were increased in combined injury at 48 hours postinjury compared with all other treatment groups. Prolonged overproduction of proinflammatory cytokines could contribute to subsequent organ damage. Decreased leukocytes might exacerbate immune impairment and susceptibility to infections. Future studies will determine whether there are long lasting consequences of this early proinflammatory response and extended decrease in leukocytes.

摘要

在核事件(如核电站熔毁事故或核攻击)后,可能会发生辐射与烧伤合并伤。对于合并伤导致死亡率高于单一损伤的机制,人们了解甚少,而且辐射与烧伤合并伤的动物模型也很少。在此,作者建立了一种辐射与烫伤合并伤的小鼠模型。给小鼠单独给予0、2、4、5、6或9格雷(Gy)的单次剂量辐射,随后进行15%体表面积的烫伤。所有接受≤4 Gy辐射并伴有烧伤的小鼠在合并伤后存活。更高剂量的辐射(5、6和9 Gy)后再进行烫伤,死亡率呈剂量依赖性增加(分别为34%、67%和100%)。确定5 Gy是该模型中与烧伤合并使用的理想剂量。与假手术组相比,烧伤、辐射及合并伤(5 Gy与烧伤)小鼠在伤后48小时循环白细胞减少(分别为49.7%、11.6%和57.3%)。与所有其他治疗组相比,合并伤小鼠在伤后48小时循环白细胞介素-6和肿瘤坏死因子-α增加。促炎细胞因子的长期过度产生可能导致随后的器官损伤。白细胞减少可能会加剧免疫损害和感染易感性。未来的研究将确定这种早期促炎反应和白细胞持续减少是否会产生长期后果。

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Influence of sublethal total-body irradiation on immune cell populations in the intestinal mucosa.亚致死全身照射对肠道黏膜免疫细胞群体的影响。
Radiat Res. 2010 Apr;173(4):469-78. doi: 10.1667/RR1742.1.
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Wound trauma increases radiation-induced mortality by activation of iNOS pathway and elevation of cytokine concentrations and bacterial infection.创伤会通过激活 iNOS 途径、提高细胞因子浓度和引发细菌感染,增加辐射诱导的死亡率。
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The somatostatin analog SOM230 (pasireotide) ameliorates injury of the intestinal mucosa and increases survival after total-body irradiation by inhibiting exocrine pancreatic secretion.生长抑素类似物SOM230(帕西瑞肽)通过抑制胰腺外分泌减轻肠黏膜损伤并提高全身照射后的生存率。
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Medical countermeasures for radiation combined injury: radiation with burn, blast, trauma and/or sepsis. report of an NIAID Workshop, March 26-27, 2007.辐射复合伤的医学对策:辐射与烧伤、爆炸伤、创伤和/或脓毒症。美国国立过敏与传染病研究所研讨会报告,2007年3月26 - 27日
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Effects of ethanol on pulmonary inflammation in postburn intratracheal infection.乙醇对烧伤后气管内感染时肺部炎症的影响。
J Burn Care Res. 2008 Mar-Apr;29(2):323-30. doi: 10.1097/BCR.0b013e3181667599.
7
The 9-11 Commission's invitation to imagine: a pathophysiology-based approach to critical care of nuclear explosion victims.9·11委员会关于设想的邀请:一种基于病理生理学的核爆炸受害者重症护理方法。
Crit Care Med. 2007 Mar;35(3):716-23. doi: 10.1097/01.CCM.0000257328.31668.22.
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Effects of serum from rats with combined radiation-burn injury on the growth of hematopoietic progenitor cells.复合辐射烧伤大鼠血清对造血祖细胞生长的影响。
J Trauma. 2007 Jan;62(1):193-8. doi: 10.1097/01.ta.0000215434.24726.72.
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Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):890-8. doi: 10.1016/j.ijrobp.2006.03.025.