烟花火药爆炸复合烧伤对大鼠心肌损伤的初步研究
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摘要
目的：初步探讨烟花火药爆炸复合烧伤大鼠心肌损伤及可能机制。
材料与方法：Wistar大鼠128只，随机分为正常对照组(n=8)、烧伤组(n=40)、爆炸伤组(n=40)和复合伤组(n=40)，分别造成大鼠20％体表面积度烧伤、火药爆炸伤和两者复合伤。动态观察大鼠伤后1、3、6、12、24小时血浆CK～MB，心肌组织含水量；心肌细织内皮素(ET)、一氧化氮(NO)、丙二醛(MDA)含量、肿瘤坏死因子α(TNF-α)含量、髓过氧化物酶(MPO)活性；心肌组织光镜、电镜形态学变化；并对各因素之间进行相关分析。
结果：复合伤组较单因素致伤组大鼠血浆CK—MB升高明显，心肌组织水肿加重，心肌组织ET含量、NO含量、MDA含量、MPO活性、TNF-α含量升高，形态学损伤更为明显，而以上因素在烧伤组和爆炸伤组间差异不明显。相关性分析提示CK-MB，ET／NO，MPO，MDA，心肌含水量，TNF-α之间两两均有正相关关系。
结论：1．烧伤、火药爆炸伤、两者复合伤均能引起心肌的损害，复合伤组心肌损伤重于单一伤。2．烟花火药爆炸复合烧伤能引起心肌血供氧供障碍，能量代谢紊乱；心肌中性粒细胞浸润，炎细胞代谢紊乱；氧自由基代谢紊乱；炎症介质(TNF-α)的异常增高等机制导致心肌损害。3．复合伤后心肌ET，NO，MPO，MDA，TNF-α异常增高比单一伤明显。4．烧伤和火药爆炸伤后在以上损伤机制方面的异常无本质差异。
Objective: To investigate the injury of cardiac muscle in rats following combined powder explosive and burn injury and its possible pathogenesis. Methods: 128 Wistar rats were randomly divided into four groups which were normal control group (n=8), burn group (n=40), powder explosive group (n=40), combined powder explosive and burn group (n=40). The latter three groups were more divided into 1, 3, 6, 12, 24 hour post injury group, and in each sub group, the animal number is 8. The latter three groups were subjected to 20% total body surface area full thickness burn injury, powder explosive injury and combined powder explosive and burn injury respectively. The following of each group were examined and studied: the CK -MR activities of the blood plasma ,the water contents of the cardiac muscle, the MDA,RT,NO, TNF- a contents and MPO activities in myocardium; the histological and ultrastructural cardiac pathology changes, and correlation analysis were made between each of the two factors.
Results: Compared with burn group and powder explosive group, the combined powder explosive and burn group's CK -MB activities of the blood plasma ,the water contents of the cardiac muscle, ET,NO,MDA, TNF- a contents and MPO activities in the heart, were all elevated significantly, and the histological and ultrastructural cardiac pathology changes were more severe. As to the above several factors, there was no essential difference between burn group and powder explosive group, the relationship between each of the two factors in CK -MB ,ET/NO,MDA, MPO, TNF- a was significance.
Conclusions: 1 .The rat's myocardial injury was obvious after burn, powder explosive, combined powder explosive and burn injury. The degree of combined wound was more severe than the above two single wound. 2.There was myocardiac injury after combined burn and powder explosive injury, It could cause the deficiency of the oxygen and blood supply of the cardiac muscle, the confusion of the energy metabolism, the infiltration of neutrophil in cardiac muscle, the confusion of the oxygen-derived free radicals, the abnormal increase of the inflammation medium(TNF- a ).3.The increase of the ET, NO, MPO, MDA, TNF?a were more obvious after the combined powder explosive and burn injury than single injury.4. As to the above several factors, there was no essential difference between burn group and powder explosive group.
材料与方法：Wistar大鼠128只，随机分为正常对照组(n=8)、烧伤组(n=40)、爆炸伤组(n=40)和复合伤组(n=40)，分别造成大鼠20％体表面积度烧伤、火药爆炸伤和两者复合伤。动态观察大鼠伤后1、3、6、12、24小时血浆CK～MB，心肌组织含水量；心肌细织内皮素(ET)、一氧化氮(NO)、丙二醛(MDA)含量、肿瘤坏死因子α(TNF-α)含量、髓过氧化物酶(MPO)活性；心肌组织光镜、电镜形态学变化；并对各因素之间进行相关分析。
结果：复合伤组较单因素致伤组大鼠血浆CK—MB升高明显，心肌组织水肿加重，心肌组织ET含量、NO含量、MDA含量、MPO活性、TNF-α含量升高，形态学损伤更为明显，而以上因素在烧伤组和爆炸伤组间差异不明显。相关性分析提示CK-MB，ET／NO，MPO，MDA，心肌含水量，TNF-α之间两两均有正相关关系。
结论：1．烧伤、火药爆炸伤、两者复合伤均能引起心肌的损害，复合伤组心肌损伤重于单一伤。2．烟花火药爆炸复合烧伤能引起心肌血供氧供障碍，能量代谢紊乱；心肌中性粒细胞浸润，炎细胞代谢紊乱；氧自由基代谢紊乱；炎症介质(TNF-α)的异常增高等机制导致心肌损害。3．复合伤后心肌ET，NO，MPO，MDA，TNF-α异常增高比单一伤明显。4．烧伤和火药爆炸伤后在以上损伤机制方面的异常无本质差异。
Objective: To investigate the injury of cardiac muscle in rats following combined powder explosive and burn injury and its possible pathogenesis. Methods: 128 Wistar rats were randomly divided into four groups which were normal control group (n=8), burn group (n=40), powder explosive group (n=40), combined powder explosive and burn group (n=40). The latter three groups were more divided into 1, 3, 6, 12, 24 hour post injury group, and in each sub group, the animal number is 8. The latter three groups were subjected to 20% total body surface area full thickness burn injury, powder explosive injury and combined powder explosive and burn injury respectively. The following of each group were examined and studied: the CK -MR activities of the blood plasma ,the water contents of the cardiac muscle, the MDA,RT,NO, TNF- a contents and MPO activities in myocardium; the histological and ultrastructural cardiac pathology changes, and correlation analysis were made between each of the two factors.
Results: Compared with burn group and powder explosive group, the combined powder explosive and burn group's CK -MB activities of the blood plasma ,the water contents of the cardiac muscle, ET,NO,MDA, TNF- a contents and MPO activities in the heart, were all elevated significantly, and the histological and ultrastructural cardiac pathology changes were more severe. As to the above several factors, there was no essential difference between burn group and powder explosive group, the relationship between each of the two factors in CK -MB ,ET/NO,MDA, MPO, TNF- a was significance.
Conclusions: 1 .The rat's myocardial injury was obvious after burn, powder explosive, combined powder explosive and burn injury. The degree of combined wound was more severe than the above two single wound. 2.There was myocardiac injury after combined burn and powder explosive injury, It could cause the deficiency of the oxygen and blood supply of the cardiac muscle, the confusion of the energy metabolism, the infiltration of neutrophil in cardiac muscle, the confusion of the oxygen-derived free radicals, the abnormal increase of the inflammation medium(TNF- a ).3.The increase of the ET, NO, MPO, MDA, TNF?a were more obvious after the combined powder explosive and burn injury than single injury.4. As to the above several factors, there was no essential difference between burn group and powder explosive group.
引文
1．汪昌荣，陈旭林．40例火药爆炸烧伤死因分析．安徽医科大学学报，1999，34(5)：396-397
2. Xu-Lin Chen, Yong-Jie Wang, Chang-Rong Wang et al. Burns due to gunpowder explosions in fireworks factory: a 13-year retrospective study. Burns 28(2002)245-249.
3．黄跃生，黎鳌，杨宗城．烧伤病人心肌损害及其机理的临床探讨．中华整形烧伤外科杂志，1993，9(2)：99—102．
4. Nabil M. Elsayed. Toxicology of blast overpressure. Toxicology 2(1997)1-15.
5. Maria A. Mayorga. The pathology of primary blast overpressure injury. Toxicology 2(1997)17-28.
6．陈发明．烧烫伤动物模型的研制．见：黎整主编．实验烧伤外科学．第一版．理庆：重庆大学出版社，1997．39-40．
7．朱佩芳．烧伤实验动物方法学．见：黎鳌主编．烧伤治疗学．第二版．北京：人
民卫生出版社，1999．650-657．
8．罗武生，郭兆贵．用髓过氧化物酶法定量测定心肌组织中的中性粒细胞．中国药理学通报，1990，6：264-269．
9．姜东锯．可乐定对小鼠及大鼠烫伤后水肿形成的抑制作用．中国药理通报．1989，10(6)：540—543．
10. Gavino VG, Miller JS. Effects of polyunsaturated fatty acid and antioxidants on lipid. J Lipid Res, 1981,22(3): 763-770.
11．迟路湘，杨宗城．烧伤后心功能不全．见：黎鳌主编．黎鳌烧伤学．第一版．上海：上海科学技术出版社，2001：349．
12．夏照帆，田建广，唐洪泰等．烫伤大鼠心肌收缩功能与细胞内游离钙的研究．中华烧伤杂志．2001，17(6)：342—344．
13．迟路湘，杨宗城，黎鳌等．大鼠严重烧伤后早期心肌血流量及其病理学基础研究．第三军医大学学报．1998，20(2)：111—113．
14．方林森．烟花火药爆炸伤106例临床分析．安徽医学，1999，20(5)：26-27．
15．程天明．瓦斯爆炸烧伤．见：黎鳌主编．烧伤治疗学．第二版．北京：人民卫生出版社，1999，347．
16. Bhayana V, Ralph Henderson A. Biochemical markers of Myocardial Damage. Clin Biochem, 1995,28(1):1-29.
17．张会堂，王甲汉．烫伤大鼠休克期不同时间切痂对心肌损伤的影响．第三军医大学学报，2001，23(2)：176—178．
18．林远，程天民，古德全等．烧冲复合伤的心脏病理变化．第三军医大学学报，1981，3(1)：19—23．
19．林远，程天民，郑怀恩等．冲击波超压致速发死亡大鼠的心脏病理变化．第三军医大学学报，1993，15(2)：141—144．．
20. Lefroy DC, Crake T, Uren NT, et al. Effect of inhibition of nitric oxide synthesis on epicardial coronary in humans. Circulation, 1993, 88(1):43-54.
21. Radi R, Beckman JS, Bush NM, et al. Peroxynitrite-induced mem-brance lipid peroxidation: the cytotoxic potential of superoxide and nitric oxide. Arch Biochem
Biophys, 1991,288:481-487.
22. Ishda H, Ishimori K,Hirota Y, et al. Peroxynitrite-induced cardiac myocyte injury. Free Rad Biol Med, 1996, 20:343-350.
23. Packer MA, Murphy MP. Peroxunitrite formed by simultaneous nitric oxide and superoxide generation causes cyclosporin-A-sensitive mitochondrial calcium efflux and depolarization. Eur J Biochem, 1995,234:231-239.
24．扬建民，刘彩云，杨宗城等．内皮素和一氧化氮对烧伤早期大鼠心肌血供的影响．中国危重病急救医学，1998，10(1)：14-15．
25. Tosi MF, Stark JM, Wane C. Induction of ICAM-lexpression on human airways epithelial by inflammatory cytokines: Effects on neutrophil adhesion. Am J Respir, 1992, 7: 214.
26. Bradlay PP, Pkiebat DA, Cristensen RD, et al. Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an enzyme marker. J Invest Dermatol, 1982,78:206-213.
27．张利华，陈鸿义．去白细胞再灌注对犬心肌的保护作用．中国现代医学杂志，1999，9(1)：3—4．
28．闫柏刚，黄跃生，杨宗城等．立即与延迟切痂对烫伤大鼠若干炎症介质变化的影响．第三军医大学学报，2001，23(1)：39—41．
29．迟路湘，杨宗城，黎鳌．严重烧伤后大鼠心肌细胞膜损伤的实验研究．中国危重病急救医学，1999，11(1)：11—14．
30. Meerson FZ, Kagan VE, Kozlov YP, et al. The role of lipid peroxidation in pathogenesis of ischemic damage and the antio-xidant protection of the heart. Basic Res Cardiol, 1982, 17: 465-471.
31. Kapadia S, Torre-Amione G, Yokoyama T, et al. Soluble TNF binding proteins modulate the negative inotropic properties of TNF-alpha in vitro. Am J Physiol,1995,268(2):517-525.
32．闫柏刚，黄跃生，杨宗城等．大鼠严重烫伤并发心肌损害时肿瘤坏死因子的变化．中国危重病急救医学，1999，11(10)：579—580．
33. Huang YS, Yang ZC, Yan BG, et al. Pathogenesis of early cardiac myocyte damage after severe burns. J Trauma, 1999,46:428-432.
34. VanEyk JE, Powers F, Law W, et al Breakdown and release of myofilament proteins during ischemia and ischemia/reperfusion in rat hearts: identification of degradation products and effects on the pCa-force relation. Circ Res, 1998,82:261-271.
35. Hein S, Scheffold T, Schaper J. Ischemia induce early changes to cy-toskeletal and contractile proteins in diseased human myocardium. J Thorac Cardiovasc Surg, 1995,110:89-98.
36. Giroir B P, Horton J W, White J D, et al. Inhibition of tumor necrosis factor prevents myocardial dysfunction during burn shock, Am J Physiol, 1994, 267: 118.
37. Bachem MG, Sell KM, Melchior R, et al. Tumor necrosis factor alpha(TNF-alpha) and transforming growth factor beta 1(TGF betal)stimulate fibronection synthesis and the transdifferentiation of fat-storing cells in the rat liver into myofibroblasts. Virchows Arch, 1993,63(2): 123-130.
2. Xu-Lin Chen, Yong-Jie Wang, Chang-Rong Wang et al. Burns due to gunpowder explosions in fireworks factory: a 13-year retrospective study. Burns 28(2002)245-249.
3．黄跃生，黎鳌，杨宗城．烧伤病人心肌损害及其机理的临床探讨．中华整形烧伤外科杂志，1993，9(2)：99—102．
4. Nabil M. Elsayed. Toxicology of blast overpressure. Toxicology 2(1997)1-15.
5. Maria A. Mayorga. The pathology of primary blast overpressure injury. Toxicology 2(1997)17-28.
6．陈发明．烧烫伤动物模型的研制．见：黎整主编．实验烧伤外科学．第一版．理庆：重庆大学出版社，1997．39-40．
7．朱佩芳．烧伤实验动物方法学．见：黎鳌主编．烧伤治疗学．第二版．北京：人
民卫生出版社，1999．650-657．
8．罗武生，郭兆贵．用髓过氧化物酶法定量测定心肌组织中的中性粒细胞．中国药理学通报，1990，6：264-269．
9．姜东锯．可乐定对小鼠及大鼠烫伤后水肿形成的抑制作用．中国药理通报．1989，10(6)：540—543．
10. Gavino VG, Miller JS. Effects of polyunsaturated fatty acid and antioxidants on lipid. J Lipid Res, 1981,22(3): 763-770.
11．迟路湘，杨宗城．烧伤后心功能不全．见：黎鳌主编．黎鳌烧伤学．第一版．上海：上海科学技术出版社，2001：349．
12．夏照帆，田建广，唐洪泰等．烫伤大鼠心肌收缩功能与细胞内游离钙的研究．中华烧伤杂志．2001，17(6)：342—344．
13．迟路湘，杨宗城，黎鳌等．大鼠严重烧伤后早期心肌血流量及其病理学基础研究．第三军医大学学报．1998，20(2)：111—113．
14．方林森．烟花火药爆炸伤106例临床分析．安徽医学，1999，20(5)：26-27．
15．程天明．瓦斯爆炸烧伤．见：黎鳌主编．烧伤治疗学．第二版．北京：人民卫生出版社，1999，347．
16. Bhayana V, Ralph Henderson A. Biochemical markers of Myocardial Damage. Clin Biochem, 1995,28(1):1-29.
17．张会堂，王甲汉．烫伤大鼠休克期不同时间切痂对心肌损伤的影响．第三军医大学学报，2001，23(2)：176—178．
18．林远，程天民，古德全等．烧冲复合伤的心脏病理变化．第三军医大学学报，1981，3(1)：19—23．
19．林远，程天民，郑怀恩等．冲击波超压致速发死亡大鼠的心脏病理变化．第三军医大学学报，1993，15(2)：141—144．．
20. Lefroy DC, Crake T, Uren NT, et al. Effect of inhibition of nitric oxide synthesis on epicardial coronary in humans. Circulation, 1993, 88(1):43-54.
21. Radi R, Beckman JS, Bush NM, et al. Peroxynitrite-induced mem-brance lipid peroxidation: the cytotoxic potential of superoxide and nitric oxide. Arch Biochem
Biophys, 1991,288:481-487.
22. Ishda H, Ishimori K,Hirota Y, et al. Peroxynitrite-induced cardiac myocyte injury. Free Rad Biol Med, 1996, 20:343-350.
23. Packer MA, Murphy MP. Peroxunitrite formed by simultaneous nitric oxide and superoxide generation causes cyclosporin-A-sensitive mitochondrial calcium efflux and depolarization. Eur J Biochem, 1995,234:231-239.
24．扬建民，刘彩云，杨宗城等．内皮素和一氧化氮对烧伤早期大鼠心肌血供的影响．中国危重病急救医学，1998，10(1)：14-15．
25. Tosi MF, Stark JM, Wane C. Induction of ICAM-lexpression on human airways epithelial by inflammatory cytokines: Effects on neutrophil adhesion. Am J Respir, 1992, 7: 214.
26. Bradlay PP, Pkiebat DA, Cristensen RD, et al. Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an enzyme marker. J Invest Dermatol, 1982,78:206-213.
27．张利华，陈鸿义．去白细胞再灌注对犬心肌的保护作用．中国现代医学杂志，1999，9(1)：3—4．
28．闫柏刚，黄跃生，杨宗城等．立即与延迟切痂对烫伤大鼠若干炎症介质变化的影响．第三军医大学学报，2001，23(1)：39—41．
29．迟路湘，杨宗城，黎鳌．严重烧伤后大鼠心肌细胞膜损伤的实验研究．中国危重病急救医学，1999，11(1)：11—14．
30. Meerson FZ, Kagan VE, Kozlov YP, et al. The role of lipid peroxidation in pathogenesis of ischemic damage and the antio-xidant protection of the heart. Basic Res Cardiol, 1982, 17: 465-471.
31. Kapadia S, Torre-Amione G, Yokoyama T, et al. Soluble TNF binding proteins modulate the negative inotropic properties of TNF-alpha in vitro. Am J Physiol,1995,268(2):517-525.
32．闫柏刚，黄跃生，杨宗城等．大鼠严重烫伤并发心肌损害时肿瘤坏死因子的变化．中国危重病急救医学，1999，11(10)：579—580．
33. Huang YS, Yang ZC, Yan BG, et al. Pathogenesis of early cardiac myocyte damage after severe burns. J Trauma, 1999,46:428-432.
34. VanEyk JE, Powers F, Law W, et al Breakdown and release of myofilament proteins during ischemia and ischemia/reperfusion in rat hearts: identification of degradation products and effects on the pCa-force relation. Circ Res, 1998,82:261-271.
35. Hein S, Scheffold T, Schaper J. Ischemia induce early changes to cy-toskeletal and contractile proteins in diseased human myocardium. J Thorac Cardiovasc Surg, 1995,110:89-98.
36. Giroir B P, Horton J W, White J D, et al. Inhibition of tumor necrosis factor prevents myocardial dysfunction during burn shock, Am J Physiol, 1994, 267: 118.
37. Bachem MG, Sell KM, Melchior R, et al. Tumor necrosis factor alpha(TNF-alpha) and transforming growth factor beta 1(TGF betal)stimulate fibronection synthesis and the transdifferentiation of fat-storing cells in the rat liver into myofibroblasts. Virchows Arch, 1993,63(2): 123-130.
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