特殊环境冲击伤的伤情特点和治疗研究
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摘要
爆炸冲击波通过介质(如空气、水、土壤、岩石、钢板等)向周围传播。根据传播介质的不同,冲击伤可分为空气冲击伤、水下冲击伤和固体冲击伤。因传播介质的密度不同,可对冲击波的传播速度和冲击伤的伤情产生明显的影响。通常传播介质的密度愈高,冲击波的传播速度愈快,传播的距离愈远,冲击伤程度也愈重。
特殊环境冲击伤主要是指高原冲击伤、水下冲击伤和坦克、装甲、舱室等有限空间内的冲击伤。高原冲击伤是指发生于海拔3000m以上地区的冲击伤。高原地区空气稀薄,大气压和氧分压低,海拔4000m的大气密度约为海平面的65%,大气压和氧分压约相当于海平面的61%,这种高原环境特点对冲击伤伤情有何影响,目前尚不十分清楚。水的密度约为空气的800倍,几乎不可被压缩,水下冲击波的传播速度远较空气冲击波快得多,衰减更慢,传播的距离也更远,传播速度约为空气中的3～4倍,炸药水下爆炸时产生的冲击波强度是其在空气中爆炸强度的3倍。同质量的TNT地面爆炸与水下爆炸相比,同距离的压力值可相差200倍左右。这种水下冲击波的物理特性对水下冲击伤伤情特点有何影响和如何进行针对性治疗也缺乏详细的研究。为此,针对未来局部冲突的热点地区,本研究重点探讨特殊环境冲击伤中的高原和水下冲击伤的伤情特点和治疗研究。
本研究在复制不同海拔高度大鼠高原冲击伤和犬、兔水下冲击伤模型的基础上,从大体、细胞和分子水平不同层次上较系统地探讨了高原和水下冲击伤的伤情特点和治疗效果。得到的主要结果和结论如下:
1.高原冲击伤的靶器官仍为肺,具有伤情重、发展快和死亡率高等特点,且随海拔高度的升高,伤情更为严重。肺损伤主要表现为出血和水肿,其程度较平原冲击伤加重1～3级。海拔390m、3500m、4000m和5000m冲击波暴露的动物,重度和极重度肺出血的发生率分别为16.7%、43.3%、60.0%和73.3%,重度和极重度肺水肿的发生率分别为6.6%、13.3%、33.3%和40.0%,死亡率分别为0%、0%、20%和40%,且死亡均发生在冲击波暴露后3h内。
2.高原(海拔4000m)冲击伤后,肺组织中IL-6、IL-10、TNF-a含量明显升高,HO-1mRNA表达明显增加,支气管肺泡灌洗液总蛋白浓度显著升高,PaO_2明显下降,提示上述细胞因子和HO-1在高原冲击伤的发生、发展过程中可能起着重要的作用。
3.高原(海拔4000m)冲击伤后给予HO-1诱导剂氯化高铁血红素hemin和地塞米松治疗可提高肺组织中IL-10含量,降低IL-6、TNF-a含量,HO-1mRNA表达增加,肺泡灌洗液总蛋白含量降低,PaO_2升高。提示上述治疗措施可减轻肺部炎性反应,对机体起到一定的保护作用,但对极重度肺冲击伤的治疗作用有限。
4.阐明了水下冲击伤的伤情特点。水下冲击伤的靶器官仍为肺,具有肺和肠道损伤发生率高、含液脏器(膀胱、胆囊等)损伤发生率低,肝脾等实质脏器损伤轻微,外轻内重表现更为典型和伤情重,死亡率高(31.58%)等特点。
5.提出了水下冲击伤的预警指标,凡水下冲击伤后出现呼吸窘迫、心动过缓、体温下降后不回升或无明显回升,提示伤情严重,这对群体水下冲击伤伤员的分类和救治具有重要指导意义。
6.水下冲击伤后给予复温、地塞米松、山莨菪碱及复温联合应用地塞米松和山莨菪碱治疗,可改善通气功能、生命体征和预后,其中以复温联合应用地塞米松和山莨菪碱治疗效果更好。
Explosion wave spreads through the mediator(namely air , water , soil, rock, steel et al). According to the different mediator, blast injury can be divided into air blast injury, underwater blast injury and solid blast injury. In different density of the mediator ,there is visible effect on spread velocity of blast wave and traumatic condition of blast injury. Usually, the higher density, faster and father the spread velocity of the blast wave propagates and more severity of the blast injury will be.
The blast injury at special environment mainly includes the blast injury at high attitude , underwater and in an enclosed space(namely tank , armored vehicle, cabin, et al). Blast injury at high attitude occurs at the region of 3000 meters height above sea level. There are scarce air, low barometric pressure and low partial pressure of oxygen. Comparing with the area of sea level, there are only 65% atmosphere density and 61% barometric pressure and partial oxygen pressure in the region of height above sea level 4000 meters. What influence on the characteristics of the blast injury in high attitude environment is still unknown by now . The density of water is 800 times as that of air. Because water is less compressible, an underwater blast wave propagates at high speeds and loses energy less quickly over longer distances. It is estimated that an explosion underwater is approximately three times greater in strength than that which is detonated in the air. The propagating velocity of underwater blast wave is 3～4 times as that of air blast wave. The pressure force is 200 times greater underwater at the same distance from the explosion when TNT of the same quantity exploses under water and in the air. So study emphasis on exploring the characteristics and interventions of the blast injury in special environment (the blast injury at high attitude and underwater blast injury ) with regard to region conflict hot spot area.
The present study systemically observed the characteristics and interventions of the blast injury at high attitude and underwater from general, cellular and molecular level based on duplicating the rat blast injury at different attitude and the dog and rabbit underwater blast injury. The main results of the present report are as following:
1. The lung was still the main injured target orgen in blast injury at high attitude. The blast injury at high attitude had the characteristics of more severity, fast developing and high mortality . Furthermore, the severity of injuries was increased with rising of the attitude . the most common injury to the lung was hemorrhage and edema, which are 1～3 degree more in severity .than that of the blast injury at plain. When the blast injury occurred at 390meters , 3500meters level ,4000 meters level and 5000 meters level, incidence of severe and very severe hemorrhage of the lung was 16.7%, 43.3%, 60.0%, and 73.3% , respectively, incidence of severe and very severe edema of the lung was 6.6%,13.3%,33.3% and 40.0% ,respectively ; the mortality was 0%, 0%, 20% and 40% respectively; And the mortality occured in 3 hours after injury.
2. After blast injury at high attitude(4000 meters) , IL-6,IL-10,TNF-a of the lung tissue were all remarkably increased. The expression of HO-1 mRNA was increased, too. The total protein of the bronchoalveolar lavage fluid was remarkably increased . Arterial oxygen tension (PaO_2)was remarkably decreased .These indicate that the cytokines mentioned above and HO-1 may play an important role in the occurance and development of the blast injury at high attitude .
3. The hemin, inductor of HO-1and dexamethason were used to treat the high attitude blast injuried rats. The result showed that they could increase the level of IL-10 of the lung , HO-1 expression and arterial oxygen tension (PaO_2). decrease the level of IL-6 and TNF-a and the total protein of the bronchoalveolar lavage fluid ; All these indicate that the treatment mentioned above could relieve the inflammatory reaction of the lung, which could be protective for the organism to some degree though they had limited effect on very severe blast injury .
4. The characteristics of underwater blast injury were explored systemically. The lung was still the main target orgen. Underwater blast injury had the characteristics of high incidence of lung and intestinal tract injuries , low incidence to fluid-filled organs injuries(namely the bladder, the cholecystis, et al), little effect on solid organs(namely the liver ,the spleen ,et al), more typical appearance of light injury outside and severe injury inside, more severity and high mortality(31.58%)et al.
5. The warning markers were recommended. It should indicate the severity of the injury when distress of respiratory, brady cardia , no rising or no obvious rising after temperature drop after underwater blast injury appeard. This may be importance to classify and treat the underwater blast injuried patients .
6. rewarming, dexamethasone and anisodamine were used to treat the underwater blast injury , respectively. The results showed that all of these could improve pulmonment function , vital sign and prognostic。Among these , combining of these factors had better intervention effects.
特殊环境冲击伤主要是指高原冲击伤、水下冲击伤和坦克、装甲、舱室等有限空间内的冲击伤。高原冲击伤是指发生于海拔3000m以上地区的冲击伤。高原地区空气稀薄,大气压和氧分压低,海拔4000m的大气密度约为海平面的65%,大气压和氧分压约相当于海平面的61%,这种高原环境特点对冲击伤伤情有何影响,目前尚不十分清楚。水的密度约为空气的800倍,几乎不可被压缩,水下冲击波的传播速度远较空气冲击波快得多,衰减更慢,传播的距离也更远,传播速度约为空气中的3～4倍,炸药水下爆炸时产生的冲击波强度是其在空气中爆炸强度的3倍。同质量的TNT地面爆炸与水下爆炸相比,同距离的压力值可相差200倍左右。这种水下冲击波的物理特性对水下冲击伤伤情特点有何影响和如何进行针对性治疗也缺乏详细的研究。为此,针对未来局部冲突的热点地区,本研究重点探讨特殊环境冲击伤中的高原和水下冲击伤的伤情特点和治疗研究。
本研究在复制不同海拔高度大鼠高原冲击伤和犬、兔水下冲击伤模型的基础上,从大体、细胞和分子水平不同层次上较系统地探讨了高原和水下冲击伤的伤情特点和治疗效果。得到的主要结果和结论如下:
1.高原冲击伤的靶器官仍为肺,具有伤情重、发展快和死亡率高等特点,且随海拔高度的升高,伤情更为严重。肺损伤主要表现为出血和水肿,其程度较平原冲击伤加重1～3级。海拔390m、3500m、4000m和5000m冲击波暴露的动物,重度和极重度肺出血的发生率分别为16.7%、43.3%、60.0%和73.3%,重度和极重度肺水肿的发生率分别为6.6%、13.3%、33.3%和40.0%,死亡率分别为0%、0%、20%和40%,且死亡均发生在冲击波暴露后3h内。
2.高原(海拔4000m)冲击伤后,肺组织中IL-6、IL-10、TNF-a含量明显升高,HO-1mRNA表达明显增加,支气管肺泡灌洗液总蛋白浓度显著升高,PaO_2明显下降,提示上述细胞因子和HO-1在高原冲击伤的发生、发展过程中可能起着重要的作用。
3.高原(海拔4000m)冲击伤后给予HO-1诱导剂氯化高铁血红素hemin和地塞米松治疗可提高肺组织中IL-10含量,降低IL-6、TNF-a含量,HO-1mRNA表达增加,肺泡灌洗液总蛋白含量降低,PaO_2升高。提示上述治疗措施可减轻肺部炎性反应,对机体起到一定的保护作用,但对极重度肺冲击伤的治疗作用有限。
4.阐明了水下冲击伤的伤情特点。水下冲击伤的靶器官仍为肺,具有肺和肠道损伤发生率高、含液脏器(膀胱、胆囊等)损伤发生率低,肝脾等实质脏器损伤轻微,外轻内重表现更为典型和伤情重,死亡率高(31.58%)等特点。
5.提出了水下冲击伤的预警指标,凡水下冲击伤后出现呼吸窘迫、心动过缓、体温下降后不回升或无明显回升,提示伤情严重,这对群体水下冲击伤伤员的分类和救治具有重要指导意义。
6.水下冲击伤后给予复温、地塞米松、山莨菪碱及复温联合应用地塞米松和山莨菪碱治疗,可改善通气功能、生命体征和预后,其中以复温联合应用地塞米松和山莨菪碱治疗效果更好。
Explosion wave spreads through the mediator(namely air , water , soil, rock, steel et al). According to the different mediator, blast injury can be divided into air blast injury, underwater blast injury and solid blast injury. In different density of the mediator ,there is visible effect on spread velocity of blast wave and traumatic condition of blast injury. Usually, the higher density, faster and father the spread velocity of the blast wave propagates and more severity of the blast injury will be.
The blast injury at special environment mainly includes the blast injury at high attitude , underwater and in an enclosed space(namely tank , armored vehicle, cabin, et al). Blast injury at high attitude occurs at the region of 3000 meters height above sea level. There are scarce air, low barometric pressure and low partial pressure of oxygen. Comparing with the area of sea level, there are only 65% atmosphere density and 61% barometric pressure and partial oxygen pressure in the region of height above sea level 4000 meters. What influence on the characteristics of the blast injury in high attitude environment is still unknown by now . The density of water is 800 times as that of air. Because water is less compressible, an underwater blast wave propagates at high speeds and loses energy less quickly over longer distances. It is estimated that an explosion underwater is approximately three times greater in strength than that which is detonated in the air. The propagating velocity of underwater blast wave is 3～4 times as that of air blast wave. The pressure force is 200 times greater underwater at the same distance from the explosion when TNT of the same quantity exploses under water and in the air. So study emphasis on exploring the characteristics and interventions of the blast injury in special environment (the blast injury at high attitude and underwater blast injury ) with regard to region conflict hot spot area.
The present study systemically observed the characteristics and interventions of the blast injury at high attitude and underwater from general, cellular and molecular level based on duplicating the rat blast injury at different attitude and the dog and rabbit underwater blast injury. The main results of the present report are as following:
1. The lung was still the main injured target orgen in blast injury at high attitude. The blast injury at high attitude had the characteristics of more severity, fast developing and high mortality . Furthermore, the severity of injuries was increased with rising of the attitude . the most common injury to the lung was hemorrhage and edema, which are 1～3 degree more in severity .than that of the blast injury at plain. When the blast injury occurred at 390meters , 3500meters level ,4000 meters level and 5000 meters level, incidence of severe and very severe hemorrhage of the lung was 16.7%, 43.3%, 60.0%, and 73.3% , respectively, incidence of severe and very severe edema of the lung was 6.6%,13.3%,33.3% and 40.0% ,respectively ; the mortality was 0%, 0%, 20% and 40% respectively; And the mortality occured in 3 hours after injury.
2. After blast injury at high attitude(4000 meters) , IL-6,IL-10,TNF-a of the lung tissue were all remarkably increased. The expression of HO-1 mRNA was increased, too. The total protein of the bronchoalveolar lavage fluid was remarkably increased . Arterial oxygen tension (PaO_2)was remarkably decreased .These indicate that the cytokines mentioned above and HO-1 may play an important role in the occurance and development of the blast injury at high attitude .
3. The hemin, inductor of HO-1and dexamethason were used to treat the high attitude blast injuried rats. The result showed that they could increase the level of IL-10 of the lung , HO-1 expression and arterial oxygen tension (PaO_2). decrease the level of IL-6 and TNF-a and the total protein of the bronchoalveolar lavage fluid ; All these indicate that the treatment mentioned above could relieve the inflammatory reaction of the lung, which could be protective for the organism to some degree though they had limited effect on very severe blast injury .
4. The characteristics of underwater blast injury were explored systemically. The lung was still the main target orgen. Underwater blast injury had the characteristics of high incidence of lung and intestinal tract injuries , low incidence to fluid-filled organs injuries(namely the bladder, the cholecystis, et al), little effect on solid organs(namely the liver ,the spleen ,et al), more typical appearance of light injury outside and severe injury inside, more severity and high mortality(31.58%)et al.
5. The warning markers were recommended. It should indicate the severity of the injury when distress of respiratory, brady cardia , no rising or no obvious rising after temperature drop after underwater blast injury appeard. This may be importance to classify and treat the underwater blast injuried patients .
6. rewarming, dexamethasone and anisodamine were used to treat the underwater blast injury , respectively. The results showed that all of these could improve pulmonment function , vital sign and prognostic。Among these , combining of these factors had better intervention effects.
引文
1. Frykberg, ER and Tepas, J.Ⅲ.1988. Terrorist bombing:Lessons learned rom Beltast to Beirut.Ann.surg.208:569-576.
2. Frykberg, ER;Hutton ,P.M; and Balzer, R.H.Jr. 1987.Disaster in Beirut:An application of mass casualty principles.Med.152:563-566.
3. Pyper P.C.,and Graham,W.J.H.1982.Analysis OF terrorist injuries treated at Craigavon Atea Hospital, Northern Ireland .Injury 14:332-338
4. Hadden,W.A.;Rutherford, W.H.; and Merrett,J.D.1978.The injuries of terrorist bombing: A study of 1532 consecutive patients.Br.J.Surg.65:525-531
5. Roy,K.1982Gunshot and bomb blast injuries: A review of experience in Belfast. J.r.society Med.75.542-545
6.王正国.原发冲击伤.人民军医,1986;(2):5.
7.王正国,杨志焕,冷华光,等.冲击伤的实验研究.中华医学杂志,1989;69(1):7.
8.赵敏,王正国,唐承功,等.犬冲击伤早期血液流变学的变化.生物医学工程杂志,1992:9(2):127.
9.尹友国,杨志焕,朱佩芳,等.犬冲击伤早期血液流变学的变化.生物医学工程杂志, 1992:(2)127.
10. Damon EG Gaylord CS, Yelverton JT et al. The effects of ambient pressure on tolerance of mammals to air blast. Aerospace Med. 1968, 39: 1039-1047.
11.杨志焕,李晓炎,朱佩芳等.高原冲击伤的损伤特点研究.西南国防医学2003,13 (1): 3-6
12.邓志龙,杨志焕,王正国等.高原冲击波致伤平台的建立及其初步应用.创伤外科杂志, 2007, 9(4): 377-378
13. Clemedson CJ.An experimental study on air blast injurier. Acta Physiol Scan 1949; 18Suppl LXI
14. Richmond DR,Clare VR, Glodizen VC, et. Biological effects of overpressure . A shock tube utilized to produce sharp-rising overpressure of 400 millisecond duration and its employment in biomedical experiments . Aerospace Med 1961;32(11):997-1008
15.王正国.冲击伤伤情的病理判断标准.科研资料汇编1976;5:73-75
16.孙立英.胸部冲击伤发生机制的实验研究.第三军医大学博士论文1990年
17. Colonel Russ Zajtchuk.MC. Conventional Warfare Ballistic ,Blast,and Burn Injuries. The Office of the Surgeon General at TMM Pubications, Center of Excellence in Mititary Medical Research and Education Walter Reed Army Medical Center Washington,D.C.20307 5000.1990
18.王正国.冲击伤救治的现代认识.人民军医, 1994;416(7):8
19.王正国.冲击伤.人民军医出版社.北京.1983
20.张均奎.冲击波负压致伤作用和致伤激励的研究.第三军医大学博士论文1992年
21. Damon EG, Gaylord CS, Hicks William, et al. The effects of ambient pressure on tolerance of mammals to air blast .DASA 1852 1996.8.
22.李天麟主编高原与健康北京科学技术出版社. 2001.73-78
23.高钰琪主编高原军事医学重庆出版社. 2005. 5
1. Dinarello CA. Proinflammatory cytokines. Chest, 2000, 118(2): 503.
2. Grellner W, Gerorg T, Wilske J. Quantitative analysis of proinflammatory cytokines (IL-1beta,IL-6,TNF-alpha) in human skin wounds. Forensic SciInt, 2000, 113 (13): 251.
3. Vincent Jl,Batter J,Marecaux G,et al.Administration of anti-TNF antibody improves left ventricylar function in septics shok patients; Result of③pilot study J.Chest, 992,101:810-815
4. Arand M,Melzner H,KinzlL,et al.Early inflammatory mediator response following isolated traumatic brain injury and other major trauma in humans J.L genbecks Arch Surg,2001,386(4):241.
5. Spielmann S,Kerner T,Ahlers o,et al.Early detection of increase tumour b necrosis factor alpha(TNF2α) and solubleTNF receptor protein plasma levels after trauma reveals associations with the clinical course J.Act a Anaesthes io logic a Scandinavica, 2001,45(3):364.
6.方步武,邱奇,吴咸中,等.急腹症并发多器官功能障碍综合征细胞因子及炎症介质与肽类激素的变化J.中国危重病急救医学,2003,15(1):19.
7. Youker K,Smith CW,Anderson DC,et al. Neutrophil adherence to isolated adult cardiac myocytes. Induction by cardia lymph collected during ischemia and reperfusion. J Clin Invest,1992,89(2):602-609.
8. Pape HC,Van Griensven M,Rice J,et al. Major secondary surgery in blunt trauma patients and perioperative cytokine liberation:determination of the clinical relevance of biochemical markers.J Trauma,2001,50(6):989-1000.
9. PROCTOR M C,SULLIVAN V,ZAJKOWSHI P,et a1.A role for interleukin-10 in the assessment of venous thromboembolism risk in injured patients[J].J Trauma,2006,60:147-151
10. MOCELLIN S,MARINCOLA F M,YOUNG H A.In.terleukin-10 and the immune response against cancer:a counterpoint[J].J Leukoc Biol,2005,78(5):1043—105
11.陈莉,赵金垣.一种新的细胞信息分子一氧化碳[J].中华内科杂志,1999,38(4): 270-272.
12. Glasgow SC, Ramachandran S, CsontosKA,et al.In terleukin-1 beta is prom inent in the early pulmonary inflammatory response after hepatic injury [J].Surgery,2005, 138(1): 6470.2
13. Li HX, Zhang JC, Zhao YL,et al.Effects of interleukin-10 on expression ofinflammatory mediators and anti-inflammatory mediators during acute lung injury in rats[J].Zhongguo Wei Zhong Bing Ji Jiu Yi Xue,2005,17(6):338341.
14. Suttner DM, Sridhar K ,Lee CS ,et al.Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells[J].Am J Physiol, 1999, 276( 3Pt 1) :443-451.
15. Suttner DM ,Dennery PA .Reversal of HO-1 related cytoprotection with increased expression is due to reactive iron[J].FASEBJ, 1999, 13:1800-1809.
16. Schipper HM ,Chertkow H , Mehindate K ,et al.Evaluation of heme oxyge nase-1 as asystemic biological marker of sporadicAD [J].Neurology,2000, 54:1297-1304.
1. Russ Zajtchuk. MC. Coventional Warefare Ballistic, Blast and Burn Injuries.The Office of the Surgeon General at TMM Publications,Center of Excellence in Military Medical Research and Education Walter Reed Army Medical Center Washington,D.C.20307 5000.1990
2. Clemedson CJ. ,Hultman H. ,Gionberg B.Respiratory and pulmonary gas exchange in blast injury. J.ApplPhysiology,1953:6:213-220
3.王正国.冲击伤.北京:人民军医出版社,1993
4. Xinmin D,Yunyou D,Chaosheng P, et al. Dexamethasone treatment attenuates earl seawater instillation-induced acute lung injury in rabbits[J]. Pharmacol, 2006, 53(4):372-379.
5. Nin N,Penuelas O,de Paula M,et al. Ventiltion-induced lung injury in rats is associated with organ injury and systemic inflammation that is atenuated by dexamethasone[J].Crit Care Med,2006,34(4):1093-1098
6. Funda A,Guniz ,M,Sibel E,et al. The effects of intratracheat dexamethasone on acute lung injury in rabbits experimental study[J].Middle East J Anesthesiol,2005,18(1): 161-171
7. Ricksen D,Liliehook B,Larsson R ,et al. Differential anti-inflammatory and anti-oxydative effects of dexamethasone and N-acetylcysteine in endotoxin-induced lung inflammttion[J].Clin Exp Immunol,2000,122(2):249-256.
8. Zampetaki A, Minamino T, Mitsialis SA,et al.Effect of heme oxygenase-1over expression in two models of lung inflammation [J].Exp Bio2l Med(Maywood),2003, 228(5):442-446.
9. Dijkstra G,B lokzijl H,Bok L,et al.Opposite effect of oxidative stress on inducible nitric oxide synthase and heme oxygenase-1 expression in intestinal inflammation:anti- inflammatory effect of carbon monoxide [J].J Pathol,2004,204(3):296-303.
10.赵晓云,郭杨,杨爽,等.内源性CO和NO在糖尿病高血压发病中关系及作用[J].山东医药. 2005,45(16):15-17.
11. Sarady JK, Zuckerbraun BS,Bilban M,et al.Carbon monoxide protection against endotoxic shock involves reciprocal effects on Inos in the lung and liver[J].FASEB J,2004,18(7):854-856.
12.王万铁,周伟斌,倪世蓉,等.HO21/CO径路在肺缺血-再灌注损伤中的作用[J].中国病理生理杂志,2005,21(9):1739.
13. Blydt-Hansen T, Katori M,Lassman C,et al.Gene transfer-induced local heme oxygenase1 overexpression protecs rat kidney transplants from ischemia/rep2erfusion injury[J]. J Am Soc Nephrol, 2003, 14(3):745.
14. Yet SF, Tian R, Layne MD, et al. Cardiac spe cific expressionof heme oxygenase-1 proctects against ischemia and reper-fusion injury in transgenic mice[J]. Cire Res, 2001,89(2):168-173.
15.周伟斌,王万铁,徐正,等.肺缺血再灌注损伤时血红素氧合酶-1的变化及意义[J].温州医学院学报,2004,34(2):94-96.
16. Katori M,Buelow R,Ke B,et al.Heme oxygenase-1 overexpression protects rat hearts from cold ischemia/reperfusion injury via an anti-apoptotic pathway [J].Transplantation, 2002,73(2):287.2
17. Suttner DM, Sridhar K, Lee CS et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells [J]. Am J Physiol, 19 9 9,27 6 ( 3Pt1) :L443-5 1.
18. Otterbein LE, Bach FH,Alam J et al. Carbon monoxide has anti-inflammation effects involving the mitogen-activated protein kinase pathway[J]. Nat Med,2000,6 ( 4) : 422-428 .
19.黄晓颖,王良兴,陈兴贤,等.一氧化碳体系对慢性肺心病大鼠肺血管结构重建的抑制作用。中华结核和呼吸杂志,2002,7:408-411
20. Morita T,Hiraka I,kurata Y ,et al. Smooth Muscle cell-derived carbon monoxide is a regular of wascular Ccgmp[j] , Proc Natl Sci USA,1995,92(5)1475-1479
21. Carraway MS,Ghio AJ, Suliman HB,et al. Txpresion of heme oxygenase -1 in the lung in chronic hypoxia [J]. .Am J Physiol Lung Cell Mol Physiol,2007,278(4):806-812
22. Christou H,Morita T,Hsieh CM, et al. Prevention of hypoxia-induced pulmonaryhypertension by inhancement of endogenous heme oxygenase-1 in ra [J].Cire Res,2000,86(12):1224-1229
23. Suttner DM , Sridhar K , Lee CS , et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygentoxicity in lung cells [J]. Am J Physiol,1999, 276 ( 3Pt 1) :443- 451.
24. Suttner DM, Dennery PA . Reversal of HO-1related cytoprotection with increased expression is due to reactiveiron[J]. FASEB J, 1999,13:1800-1809.
25. Schipper HM , Chertkow H , Mehindate K , et al. Evaluation of heme oxygenase-1 as a systemic biological marker of sporadic AD [J]. Neurology , 2000,54:1297-1304.
1. Briggs SM, Brinsfield KH. Advanced disaster medical response. Boston: Harvard Medical International Trauma & Disaster Institute;2003.
2.王正国.冲击伤.北京:人民军医出版社, 1983, 77~78.
3.宁心,李晓炎,杨志焕等.水下冲击波和空气冲击波传播速度及物理参数的对比研究.解放军医学杂志. 2004, 29(2) : 97~99.
4.杨志焕,李晓炎、宁心等.水下冲击波与空气冲击波对生物内脏损伤效应的对比研究.中华航海医学与高气压医学杂志. 2006, 13(2) : 65~68。
5. Stuhmiller JH, Phillips YY, Richmond DR. The physics and mechanism of primary blast injury. In: Bellamy RF, Jenkins DP, Zajtcjuk JT, et al, eds. Conventional warfare: ballistic, blast, and burn injuries. Washington, DC: Office of Surgeon General at TMM Publications; 1991:241–250.
6. Landsberg PG. Underwater blast injuries. Available at: http://www. scuba-doc.com/ uwblast. html. Accessed July 26,2006.
7.杨志焕,朱佩芳,蒋建新.水下冲击伤处理原则的初步探讨.创伤外科杂志. 2006, 8(3) : 234~237.
1. Phillips YY, Zaitchuk J. The management of primary blast injury.Bellamy RF, Zaichukk. Conventional Warfare Ballistics and Burn injuries—Textbook of Military Medicine (part 1, vol 5). Washington D. C. office of the Surgeon General Dept of the Army . 1991,231—232
2.杨志焕、朱佩芳、蒋建新,等.水下冲击伤的量效关系研究.解放军医学杂志,2004,29(2):95～96,102.
3.杨志焕、朱佩芳、蒋建新,等.水下冲击伤损伤特点的初步探讨.中华创伤杂志, 2003,19(2):111～114.
4.李楚杰,冷伤.北京:人民卫生出版社,1980.238～248.
5.单佑安、蒋建新、杨志焕,等.大剂量地塞米松对犬严重肺冲击伤的治疗作用.第三军医大学学报,2003,25(11):935～937.
6.岳茂兴、杨鹤鸣、王正国,等.山莨蓉碱联用地塞米松对四氧化二氮爆炸致冲毒复合伤大鼠血气的影响.中华航空肮天医学杂志,2001,12(1):35～39.
1. Wise CD,Drabkin DL . Degradation of haemoglobin and hemin to biliverdin by a new cell-free ststem obtained from the hemophagous organ of dog placenta [J]. Fed Proc,19 6 4, 23:323.
2. Llesuy SF,Tomaro ML . Heme oxygenase and oxidative stress. Evidence of involvement of bilirubin as physiological protector against oxidative damage. Biochim Biophys Acta. 19 9 4, 1223( 1) : 9 -14.
3. Poss KD,Tonegawa S. Heme oxygenase-1 isrequired for mammalian iron reutilization .Proc Natl Acad Sci. 19 9 7,9 4( 20) : 109 19 -24.
4. Dennery PA , Spitz DR , Yang G , et al. Oxygen toxicity and iron accumulationin the lungs of mice lacking hemeoxygenase-2 [J]. J Clin Invest, 1998,101( 5) :1001-11.
5. Poss KD , Tonegawa S . Reduced stress defense in heme oxygenase-1 defi cient cells[J]. Proceeding of the National Academy of Sciences of the Unit ed States of America , 1997,94:10925-10930.
6. Yachie A , Niida Y , Wada T , et al. Oxidative stress causes enhanced endothelial cellunjury in human hemeoxy genase-1 deficiency[J]. Journal of Clinical Investigation , 1999,103:129-135.
7. Otterbein LE , Bach FH , Alam J,et al. Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway[J].NatMed 2006,6:422-428.
8. Suttner DM , Dennery PA . Reversal of HO-1 related cytoprotection with increased expression is due to reactiveiron[J].FASEBJ,1999,13:1800 -1809.
9. Schipper HM , Chertkow H , MehindateK , et al. Evaluation of heme oxygenase-1 as a systemic biological marker of sporadic AD [J].Neurology , 2007, 54:1297-1304.
10. Morse D, Choi AM . Heme Oxygenase-1 The“Emerging Molecule”Has Arrived. Am JRespir Cell Mol Biol. 2002; 27 ( 1) :8 -16 .
11. Kukoba TV, Moibenko OO et al. Heme oxygenase and carbon monoxide: the protection or injury of cells? Fiziol Zh,2002, 48 ( 5 ) : 7 9 -9 2.
12. Immenschuh S, Tan M, Ramadori G et al. Nitric oxide mediates the lipopolysaccharide dependent upregulation of the heme oxygenase-1 gene expression in cultured rat Kupffer cells. J Hepatol, 19 9 9,30( 1) :6 1-9 .
13. Sang-Wook Kim, Hyun-Mee Oh, Beom-Su Kim et al. Soluble factor from tumor cells induces heme oxygenase-1 by a nitric oxide-independent mechanism in murine peritoneal macrophages[J]. Exp .Mol. Med . Vol ,2003, 35 ( 1) :5 3-9 .
14. Ishii T, Itoh K, Sato H et al. Oxidativestress-inducible proterns in macroghages[J].Free Rad Res, 19 9 9,31( 4) : 35 1-5 .
15. Brouard S, Otterbein LE, Anrather J et al. Carbon monoxide generated by heme oxygenase-1 suppress endothelial cell apoptosis[J].J Exp Med . 2000,19 2( 7 ) :1015 -25 .
16. poChoi AM,Alam J. Heme oxygenase-1: function, regulation,and im plication of a novelstress-inducible protein in oxidant-induced lung injury[J]. Am J Respir Cell Mol Biol, 199 6,15 ( 1) :9 -19 .
17. Suttner DM, Sridhar K, Lee CS et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells [J]. Am J Physiol, 19 9 9,27 6 ( 3Pt1) :L443-5 1.
18. Otterbein LE, Bach FH,Alam J et al. Carbon monoxide has anti-inflammation effects involving the mitogen-activated protein kinase pathway[J]. Nat Med,2000,6 ( 4) : 422-428 .
19.黄晓颖,王良兴,陈兴贤,等.一氧化碳体系对慢性肺心病大鼠肺血管结构重建的抑制作用。中华结核和呼吸杂志,2002,7:408-411
20. Morita T,Hiraka I,kurata Y ,et al. Smooth Muscle cell-derived carbon monoxide is a regular of wascular Ccgmp[j] , Proc Natl Sci USA,1995,92(5)1475-1479
21. Carraway MS,Ghio AJ, Suliman HB,et al. Txpresion of heme oxygenase -1 in the lung in chronic hypoxia [J]. .Am J Physiol Lung Cell Mol Physiol,2007,278(4):806-812
22. Christou H,Morita T,Hsieh CM, et al. Prevention of hypoxia-induced pulmonary hypertension by inhancement of endogenous heme oxygenase-1 in ra [J].CireRes,2000,86(12):1224-1229
23. Harju T, Soini Y, Paakko R et al. Up-regulation of heme oxygenase-1 in alveolar macrophages of newly diagnosed asth matics[J]. Respire Med. 2002, 9 6 ( 6 ) : 418 -23.
24. Chapman JT, Otterbein LE, Elias JA et al. Carbon monoxide attenuates aeroallergen-induced inflammation in mice. Am J PhysiolLung Cell Mol Physiol, 2001,28 1( 1) : L209 -16 .
25. Rodgers PA, Vreman HJ,Dennry PA,et,al. Sources of carbon monoxide (CO) in biological systems and applications of CO detection technologies[J].Semin Perinatol,1994,18(1)2-10
26. Kap turczakMH, Wasserfall C, Brusko T, et al. HemeOxygenase-1 modulates early inflammatory responses evidence from the heme oxygenase212deficient mouse [ J ]. American J Pathology, 2004,165: 1045-1053.
27. Belcher1 JD, Mahaseth H, Welch TE, et al. Heme oxygenase-1 is a modulator of inflammation and vaso occlusion in transgenic sicklemice [ J ]. J Clin Invest, 2006, 116:808-816.
28. Morita T. Heme oxygenase and atherosclerosis[ J ]. Arteriosclero2sis, Thrombosis and Vascular Biology, 2005, 25: 1786.
29. Kap itulnik J. Bilirubin: an endogenous p roduct of heme degrada2tion with both cytotoxic and cytop rotective p roperties [ J ]. MolPharmacol, 2004, 66: 773-779.
30. Wagener FA DTG, Eggert A, Boerman OC, et al. Heme is a potent inducer of inflammation in mice and is counteracted by hemeoxygenase[ J ]. Blood, 2001, 98 ( 6) : 1802-1811.
31.鲍文华,石峰,刑继强。血红素氧和酶-1/-氧化碳系统在肺纤维化大鼠中的表达及药物干预.中华实用医药,2008,5(15)39-41
1. Phillips YY, Zaitchuk J. The management of primary blast injury.Bellamy RF, Zaichukk. Conventional Warfare Ballistics and Burn injuries—Textbook of Military Medicine (part 1, vol 5). Washington D. C. office of the Surgeon General Dept of the Army . 1991,231—232
2. Yang Zhi-huan, Zhu Pei-fang, et al. Dose-effect relationship study of underwater blast injury. Medical Journal of the Liberation Army .2004,29(2):95～96,102.
3. Yang Zhi-huan, Zhu Pei-fang, et al. Study of the Injuried Characteristic of Underwater Blast Injury. Trauma Journal of China .2003,19(2):111～114.
4. Li Chu-jie. Cold Injury. The People Health Publishing Company. 1980.238～248.
5. Shan You-an, Jiang Jian-xin, et al. The Effect of Dexamethasone of Large Dose on Severe Lung Blast Injury of Dogs. The Journal of the Third Military Medical University. 2003,25(11):935～937.
6. Yue Mao-xing, Yang He-ming, et al. The Effect of Dexamethasone and Anisodamine on Blood Gas of Blast and Poisoned Injuried Lung of Rat . Aero-Medical Journal of China. 2001,12(1):35～39.
2. Frykberg, ER;Hutton ,P.M; and Balzer, R.H.Jr. 1987.Disaster in Beirut:An application of mass casualty principles.Med.152:563-566.
3. Pyper P.C.,and Graham,W.J.H.1982.Analysis OF terrorist injuries treated at Craigavon Atea Hospital, Northern Ireland .Injury 14:332-338
4. Hadden,W.A.;Rutherford, W.H.; and Merrett,J.D.1978.The injuries of terrorist bombing: A study of 1532 consecutive patients.Br.J.Surg.65:525-531
5. Roy,K.1982Gunshot and bomb blast injuries: A review of experience in Belfast. J.r.society Med.75.542-545
6.王正国.原发冲击伤.人民军医,1986;(2):5.
7.王正国,杨志焕,冷华光,等.冲击伤的实验研究.中华医学杂志,1989;69(1):7.
8.赵敏,王正国,唐承功,等.犬冲击伤早期血液流变学的变化.生物医学工程杂志,1992:9(2):127.
9.尹友国,杨志焕,朱佩芳,等.犬冲击伤早期血液流变学的变化.生物医学工程杂志, 1992:(2)127.
10. Damon EG Gaylord CS, Yelverton JT et al. The effects of ambient pressure on tolerance of mammals to air blast. Aerospace Med. 1968, 39: 1039-1047.
11.杨志焕,李晓炎,朱佩芳等.高原冲击伤的损伤特点研究.西南国防医学2003,13 (1): 3-6
12.邓志龙,杨志焕,王正国等.高原冲击波致伤平台的建立及其初步应用.创伤外科杂志, 2007, 9(4): 377-378
13. Clemedson CJ.An experimental study on air blast injurier. Acta Physiol Scan 1949; 18Suppl LXI
14. Richmond DR,Clare VR, Glodizen VC, et. Biological effects of overpressure . A shock tube utilized to produce sharp-rising overpressure of 400 millisecond duration and its employment in biomedical experiments . Aerospace Med 1961;32(11):997-1008
15.王正国.冲击伤伤情的病理判断标准.科研资料汇编1976;5:73-75
16.孙立英.胸部冲击伤发生机制的实验研究.第三军医大学博士论文1990年
17. Colonel Russ Zajtchuk.MC. Conventional Warfare Ballistic ,Blast,and Burn Injuries. The Office of the Surgeon General at TMM Pubications, Center of Excellence in Mititary Medical Research and Education Walter Reed Army Medical Center Washington,D.C.20307 5000.1990
18.王正国.冲击伤救治的现代认识.人民军医, 1994;416(7):8
19.王正国.冲击伤.人民军医出版社.北京.1983
20.张均奎.冲击波负压致伤作用和致伤激励的研究.第三军医大学博士论文1992年
21. Damon EG, Gaylord CS, Hicks William, et al. The effects of ambient pressure on tolerance of mammals to air blast .DASA 1852 1996.8.
22.李天麟主编高原与健康北京科学技术出版社. 2001.73-78
23.高钰琪主编高原军事医学重庆出版社. 2005. 5
1. Dinarello CA. Proinflammatory cytokines. Chest, 2000, 118(2): 503.
2. Grellner W, Gerorg T, Wilske J. Quantitative analysis of proinflammatory cytokines (IL-1beta,IL-6,TNF-alpha) in human skin wounds. Forensic SciInt, 2000, 113 (13): 251.
3. Vincent Jl,Batter J,Marecaux G,et al.Administration of anti-TNF antibody improves left ventricylar function in septics shok patients; Result of③pilot study J.Chest, 992,101:810-815
4. Arand M,Melzner H,KinzlL,et al.Early inflammatory mediator response following isolated traumatic brain injury and other major trauma in humans J.L genbecks Arch Surg,2001,386(4):241.
5. Spielmann S,Kerner T,Ahlers o,et al.Early detection of increase tumour b necrosis factor alpha(TNF2α) and solubleTNF receptor protein plasma levels after trauma reveals associations with the clinical course J.Act a Anaesthes io logic a Scandinavica, 2001,45(3):364.
6.方步武,邱奇,吴咸中,等.急腹症并发多器官功能障碍综合征细胞因子及炎症介质与肽类激素的变化J.中国危重病急救医学,2003,15(1):19.
7. Youker K,Smith CW,Anderson DC,et al. Neutrophil adherence to isolated adult cardiac myocytes. Induction by cardia lymph collected during ischemia and reperfusion. J Clin Invest,1992,89(2):602-609.
8. Pape HC,Van Griensven M,Rice J,et al. Major secondary surgery in blunt trauma patients and perioperative cytokine liberation:determination of the clinical relevance of biochemical markers.J Trauma,2001,50(6):989-1000.
9. PROCTOR M C,SULLIVAN V,ZAJKOWSHI P,et a1.A role for interleukin-10 in the assessment of venous thromboembolism risk in injured patients[J].J Trauma,2006,60:147-151
10. MOCELLIN S,MARINCOLA F M,YOUNG H A.In.terleukin-10 and the immune response against cancer:a counterpoint[J].J Leukoc Biol,2005,78(5):1043—105
11.陈莉,赵金垣.一种新的细胞信息分子一氧化碳[J].中华内科杂志,1999,38(4): 270-272.
12. Glasgow SC, Ramachandran S, CsontosKA,et al.In terleukin-1 beta is prom inent in the early pulmonary inflammatory response after hepatic injury [J].Surgery,2005, 138(1): 6470.2
13. Li HX, Zhang JC, Zhao YL,et al.Effects of interleukin-10 on expression ofinflammatory mediators and anti-inflammatory mediators during acute lung injury in rats[J].Zhongguo Wei Zhong Bing Ji Jiu Yi Xue,2005,17(6):338341.
14. Suttner DM, Sridhar K ,Lee CS ,et al.Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells[J].Am J Physiol, 1999, 276( 3Pt 1) :443-451.
15. Suttner DM ,Dennery PA .Reversal of HO-1 related cytoprotection with increased expression is due to reactive iron[J].FASEBJ, 1999, 13:1800-1809.
16. Schipper HM ,Chertkow H , Mehindate K ,et al.Evaluation of heme oxyge nase-1 as asystemic biological marker of sporadicAD [J].Neurology,2000, 54:1297-1304.
1. Russ Zajtchuk. MC. Coventional Warefare Ballistic, Blast and Burn Injuries.The Office of the Surgeon General at TMM Publications,Center of Excellence in Military Medical Research and Education Walter Reed Army Medical Center Washington,D.C.20307 5000.1990
2. Clemedson CJ. ,Hultman H. ,Gionberg B.Respiratory and pulmonary gas exchange in blast injury. J.ApplPhysiology,1953:6:213-220
3.王正国.冲击伤.北京:人民军医出版社,1993
4. Xinmin D,Yunyou D,Chaosheng P, et al. Dexamethasone treatment attenuates earl seawater instillation-induced acute lung injury in rabbits[J]. Pharmacol, 2006, 53(4):372-379.
5. Nin N,Penuelas O,de Paula M,et al. Ventiltion-induced lung injury in rats is associated with organ injury and systemic inflammation that is atenuated by dexamethasone[J].Crit Care Med,2006,34(4):1093-1098
6. Funda A,Guniz ,M,Sibel E,et al. The effects of intratracheat dexamethasone on acute lung injury in rabbits experimental study[J].Middle East J Anesthesiol,2005,18(1): 161-171
7. Ricksen D,Liliehook B,Larsson R ,et al. Differential anti-inflammatory and anti-oxydative effects of dexamethasone and N-acetylcysteine in endotoxin-induced lung inflammttion[J].Clin Exp Immunol,2000,122(2):249-256.
8. Zampetaki A, Minamino T, Mitsialis SA,et al.Effect of heme oxygenase-1over expression in two models of lung inflammation [J].Exp Bio2l Med(Maywood),2003, 228(5):442-446.
9. Dijkstra G,B lokzijl H,Bok L,et al.Opposite effect of oxidative stress on inducible nitric oxide synthase and heme oxygenase-1 expression in intestinal inflammation:anti- inflammatory effect of carbon monoxide [J].J Pathol,2004,204(3):296-303.
10.赵晓云,郭杨,杨爽,等.内源性CO和NO在糖尿病高血压发病中关系及作用[J].山东医药. 2005,45(16):15-17.
11. Sarady JK, Zuckerbraun BS,Bilban M,et al.Carbon monoxide protection against endotoxic shock involves reciprocal effects on Inos in the lung and liver[J].FASEB J,2004,18(7):854-856.
12.王万铁,周伟斌,倪世蓉,等.HO21/CO径路在肺缺血-再灌注损伤中的作用[J].中国病理生理杂志,2005,21(9):1739.
13. Blydt-Hansen T, Katori M,Lassman C,et al.Gene transfer-induced local heme oxygenase1 overexpression protecs rat kidney transplants from ischemia/rep2erfusion injury[J]. J Am Soc Nephrol, 2003, 14(3):745.
14. Yet SF, Tian R, Layne MD, et al. Cardiac spe cific expressionof heme oxygenase-1 proctects against ischemia and reper-fusion injury in transgenic mice[J]. Cire Res, 2001,89(2):168-173.
15.周伟斌,王万铁,徐正,等.肺缺血再灌注损伤时血红素氧合酶-1的变化及意义[J].温州医学院学报,2004,34(2):94-96.
16. Katori M,Buelow R,Ke B,et al.Heme oxygenase-1 overexpression protects rat hearts from cold ischemia/reperfusion injury via an anti-apoptotic pathway [J].Transplantation, 2002,73(2):287.2
17. Suttner DM, Sridhar K, Lee CS et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells [J]. Am J Physiol, 19 9 9,27 6 ( 3Pt1) :L443-5 1.
18. Otterbein LE, Bach FH,Alam J et al. Carbon monoxide has anti-inflammation effects involving the mitogen-activated protein kinase pathway[J]. Nat Med,2000,6 ( 4) : 422-428 .
19.黄晓颖,王良兴,陈兴贤,等.一氧化碳体系对慢性肺心病大鼠肺血管结构重建的抑制作用。中华结核和呼吸杂志,2002,7:408-411
20. Morita T,Hiraka I,kurata Y ,et al. Smooth Muscle cell-derived carbon monoxide is a regular of wascular Ccgmp[j] , Proc Natl Sci USA,1995,92(5)1475-1479
21. Carraway MS,Ghio AJ, Suliman HB,et al. Txpresion of heme oxygenase -1 in the lung in chronic hypoxia [J]. .Am J Physiol Lung Cell Mol Physiol,2007,278(4):806-812
22. Christou H,Morita T,Hsieh CM, et al. Prevention of hypoxia-induced pulmonaryhypertension by inhancement of endogenous heme oxygenase-1 in ra [J].Cire Res,2000,86(12):1224-1229
23. Suttner DM , Sridhar K , Lee CS , et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygentoxicity in lung cells [J]. Am J Physiol,1999, 276 ( 3Pt 1) :443- 451.
24. Suttner DM, Dennery PA . Reversal of HO-1related cytoprotection with increased expression is due to reactiveiron[J]. FASEB J, 1999,13:1800-1809.
25. Schipper HM , Chertkow H , Mehindate K , et al. Evaluation of heme oxygenase-1 as a systemic biological marker of sporadic AD [J]. Neurology , 2000,54:1297-1304.
1. Briggs SM, Brinsfield KH. Advanced disaster medical response. Boston: Harvard Medical International Trauma & Disaster Institute;2003.
2.王正国.冲击伤.北京:人民军医出版社, 1983, 77~78.
3.宁心,李晓炎,杨志焕等.水下冲击波和空气冲击波传播速度及物理参数的对比研究.解放军医学杂志. 2004, 29(2) : 97~99.
4.杨志焕,李晓炎、宁心等.水下冲击波与空气冲击波对生物内脏损伤效应的对比研究.中华航海医学与高气压医学杂志. 2006, 13(2) : 65~68。
5. Stuhmiller JH, Phillips YY, Richmond DR. The physics and mechanism of primary blast injury. In: Bellamy RF, Jenkins DP, Zajtcjuk JT, et al, eds. Conventional warfare: ballistic, blast, and burn injuries. Washington, DC: Office of Surgeon General at TMM Publications; 1991:241–250.
6. Landsberg PG. Underwater blast injuries. Available at: http://www. scuba-doc.com/ uwblast. html. Accessed July 26,2006.
7.杨志焕,朱佩芳,蒋建新.水下冲击伤处理原则的初步探讨.创伤外科杂志. 2006, 8(3) : 234~237.
1. Phillips YY, Zaitchuk J. The management of primary blast injury.Bellamy RF, Zaichukk. Conventional Warfare Ballistics and Burn injuries—Textbook of Military Medicine (part 1, vol 5). Washington D. C. office of the Surgeon General Dept of the Army . 1991,231—232
2.杨志焕、朱佩芳、蒋建新,等.水下冲击伤的量效关系研究.解放军医学杂志,2004,29(2):95～96,102.
3.杨志焕、朱佩芳、蒋建新,等.水下冲击伤损伤特点的初步探讨.中华创伤杂志, 2003,19(2):111～114.
4.李楚杰,冷伤.北京:人民卫生出版社,1980.238～248.
5.单佑安、蒋建新、杨志焕,等.大剂量地塞米松对犬严重肺冲击伤的治疗作用.第三军医大学学报,2003,25(11):935～937.
6.岳茂兴、杨鹤鸣、王正国,等.山莨蓉碱联用地塞米松对四氧化二氮爆炸致冲毒复合伤大鼠血气的影响.中华航空肮天医学杂志,2001,12(1):35～39.
1. Wise CD,Drabkin DL . Degradation of haemoglobin and hemin to biliverdin by a new cell-free ststem obtained from the hemophagous organ of dog placenta [J]. Fed Proc,19 6 4, 23:323.
2. Llesuy SF,Tomaro ML . Heme oxygenase and oxidative stress. Evidence of involvement of bilirubin as physiological protector against oxidative damage. Biochim Biophys Acta. 19 9 4, 1223( 1) : 9 -14.
3. Poss KD,Tonegawa S. Heme oxygenase-1 isrequired for mammalian iron reutilization .Proc Natl Acad Sci. 19 9 7,9 4( 20) : 109 19 -24.
4. Dennery PA , Spitz DR , Yang G , et al. Oxygen toxicity and iron accumulationin the lungs of mice lacking hemeoxygenase-2 [J]. J Clin Invest, 1998,101( 5) :1001-11.
5. Poss KD , Tonegawa S . Reduced stress defense in heme oxygenase-1 defi cient cells[J]. Proceeding of the National Academy of Sciences of the Unit ed States of America , 1997,94:10925-10930.
6. Yachie A , Niida Y , Wada T , et al. Oxidative stress causes enhanced endothelial cellunjury in human hemeoxy genase-1 deficiency[J]. Journal of Clinical Investigation , 1999,103:129-135.
7. Otterbein LE , Bach FH , Alam J,et al. Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway[J].NatMed 2006,6:422-428.
8. Suttner DM , Dennery PA . Reversal of HO-1 related cytoprotection with increased expression is due to reactiveiron[J].FASEBJ,1999,13:1800 -1809.
9. Schipper HM , Chertkow H , MehindateK , et al. Evaluation of heme oxygenase-1 as a systemic biological marker of sporadic AD [J].Neurology , 2007, 54:1297-1304.
10. Morse D, Choi AM . Heme Oxygenase-1 The“Emerging Molecule”Has Arrived. Am JRespir Cell Mol Biol. 2002; 27 ( 1) :8 -16 .
11. Kukoba TV, Moibenko OO et al. Heme oxygenase and carbon monoxide: the protection or injury of cells? Fiziol Zh,2002, 48 ( 5 ) : 7 9 -9 2.
12. Immenschuh S, Tan M, Ramadori G et al. Nitric oxide mediates the lipopolysaccharide dependent upregulation of the heme oxygenase-1 gene expression in cultured rat Kupffer cells. J Hepatol, 19 9 9,30( 1) :6 1-9 .
13. Sang-Wook Kim, Hyun-Mee Oh, Beom-Su Kim et al. Soluble factor from tumor cells induces heme oxygenase-1 by a nitric oxide-independent mechanism in murine peritoneal macrophages[J]. Exp .Mol. Med . Vol ,2003, 35 ( 1) :5 3-9 .
14. Ishii T, Itoh K, Sato H et al. Oxidativestress-inducible proterns in macroghages[J].Free Rad Res, 19 9 9,31( 4) : 35 1-5 .
15. Brouard S, Otterbein LE, Anrather J et al. Carbon monoxide generated by heme oxygenase-1 suppress endothelial cell apoptosis[J].J Exp Med . 2000,19 2( 7 ) :1015 -25 .
16. poChoi AM,Alam J. Heme oxygenase-1: function, regulation,and im plication of a novelstress-inducible protein in oxidant-induced lung injury[J]. Am J Respir Cell Mol Biol, 199 6,15 ( 1) :9 -19 .
17. Suttner DM, Sridhar K, Lee CS et al. Protective effects of transient HO-1 overexpression on susceptibility to oxygen toxicity in lung cells [J]. Am J Physiol, 19 9 9,27 6 ( 3Pt1) :L443-5 1.
18. Otterbein LE, Bach FH,Alam J et al. Carbon monoxide has anti-inflammation effects involving the mitogen-activated protein kinase pathway[J]. Nat Med,2000,6 ( 4) : 422-428 .
19.黄晓颖,王良兴,陈兴贤,等.一氧化碳体系对慢性肺心病大鼠肺血管结构重建的抑制作用。中华结核和呼吸杂志,2002,7:408-411
20. Morita T,Hiraka I,kurata Y ,et al. Smooth Muscle cell-derived carbon monoxide is a regular of wascular Ccgmp[j] , Proc Natl Sci USA,1995,92(5)1475-1479
21. Carraway MS,Ghio AJ, Suliman HB,et al. Txpresion of heme oxygenase -1 in the lung in chronic hypoxia [J]. .Am J Physiol Lung Cell Mol Physiol,2007,278(4):806-812
22. Christou H,Morita T,Hsieh CM, et al. Prevention of hypoxia-induced pulmonary hypertension by inhancement of endogenous heme oxygenase-1 in ra [J].CireRes,2000,86(12):1224-1229
23. Harju T, Soini Y, Paakko R et al. Up-regulation of heme oxygenase-1 in alveolar macrophages of newly diagnosed asth matics[J]. Respire Med. 2002, 9 6 ( 6 ) : 418 -23.
24. Chapman JT, Otterbein LE, Elias JA et al. Carbon monoxide attenuates aeroallergen-induced inflammation in mice. Am J PhysiolLung Cell Mol Physiol, 2001,28 1( 1) : L209 -16 .
25. Rodgers PA, Vreman HJ,Dennry PA,et,al. Sources of carbon monoxide (CO) in biological systems and applications of CO detection technologies[J].Semin Perinatol,1994,18(1)2-10
26. Kap turczakMH, Wasserfall C, Brusko T, et al. HemeOxygenase-1 modulates early inflammatory responses evidence from the heme oxygenase212deficient mouse [ J ]. American J Pathology, 2004,165: 1045-1053.
27. Belcher1 JD, Mahaseth H, Welch TE, et al. Heme oxygenase-1 is a modulator of inflammation and vaso occlusion in transgenic sicklemice [ J ]. J Clin Invest, 2006, 116:808-816.
28. Morita T. Heme oxygenase and atherosclerosis[ J ]. Arteriosclero2sis, Thrombosis and Vascular Biology, 2005, 25: 1786.
29. Kap itulnik J. Bilirubin: an endogenous p roduct of heme degrada2tion with both cytotoxic and cytop rotective p roperties [ J ]. MolPharmacol, 2004, 66: 773-779.
30. Wagener FA DTG, Eggert A, Boerman OC, et al. Heme is a potent inducer of inflammation in mice and is counteracted by hemeoxygenase[ J ]. Blood, 2001, 98 ( 6) : 1802-1811.
31.鲍文华,石峰,刑继强。血红素氧和酶-1/-氧化碳系统在肺纤维化大鼠中的表达及药物干预.中华实用医药,2008,5(15)39-41
1. Phillips YY, Zaitchuk J. The management of primary blast injury.Bellamy RF, Zaichukk. Conventional Warfare Ballistics and Burn injuries—Textbook of Military Medicine (part 1, vol 5). Washington D. C. office of the Surgeon General Dept of the Army . 1991,231—232
2. Yang Zhi-huan, Zhu Pei-fang, et al. Dose-effect relationship study of underwater blast injury. Medical Journal of the Liberation Army .2004,29(2):95～96,102.
3. Yang Zhi-huan, Zhu Pei-fang, et al. Study of the Injuried Characteristic of Underwater Blast Injury. Trauma Journal of China .2003,19(2):111～114.
4. Li Chu-jie. Cold Injury. The People Health Publishing Company. 1980.238～248.
5. Shan You-an, Jiang Jian-xin, et al. The Effect of Dexamethasone of Large Dose on Severe Lung Blast Injury of Dogs. The Journal of the Third Military Medical University. 2003,25(11):935～937.
6. Yue Mao-xing, Yang He-ming, et al. The Effect of Dexamethasone and Anisodamine on Blood Gas of Blast and Poisoned Injuried Lung of Rat . Aero-Medical Journal of China. 2001,12(1):35～39.
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