湿热环境下烫伤兔早期低氧血症的实验研究
摘要
目的：探讨高温高湿环境下烧伤兔低氧血症发生的时间、进展，分析形成原因与机制，为进一步建立南方战／地区烧伤患者低氧血症的评估标准奠定理论基础，同时也为南方战场烧伤患者呼吸功能的监护及支持提供实验依据。
方法：24只雄性新西兰兔随机分为常温无烫组(cwwt)、常温烫伤组(cwts)、高温无烫组(gwwt)和高温烫伤组(gwts)，每组6只。烫伤组动物背部及躯干两侧浸入95℃热水中30s制成30％Ⅲ度烫伤模型(Ⅲ度30％TBSA)，高温组的实验环境条件为Tdb(38±1)℃，Rh(65±5)％，常温组的实验环境条件为Tdb(24±1)℃，Rh(55±5)％。各组动物暴露时间均为120min，分别于伤前及伤后40min、80min、120min监测生命体征、动脉血气的变化，各组动物于120min处死，取肺组织做常规病理学检查。
结果：
(1) 生命体征的变化
高温无烫组和高温烫伤组动物施加干预条件后均出现Tr升高、RF和HR增快、MAP下降，各时间点组内比较差异有统计学意义(P＜0.05)；常温烫伤组烫伤后HR增快、MAP下降各时间点组内比较差异有统计学意义(P＜0.05)，但Tr、RF变化不明显，各时间点组内比较差异无统计学意义(P＞0.05)。常温无烫组各指标各时间点组内比较差异无统计学意义(P＞0.05)。各指标同时间点组间比较差异有统计学意义(P＜0.05)，其变化幅度为高温烫伤组＞高温无烫组＞常温烫伤组＞常温无烫组。
(2) 血气指标的变化
高温烫伤组PaO_2 80min开始下降，SaO_2 120min出现下降，与伤前比较差异有统计学意义(P＜0.05)，PA-aO_2和PaCO_2逐渐下降，各时间点组内比较差异有统计学意义(P＜0.05)，高温无烫组和常温烫伤组实验过
程中Pao:、SaO:变化不明显，各时间点组内比较差异无统计学意义
(P>0.05)，但PaCo:逐渐下降，PA一ao:逐渐升高，与伤前比较差异有统
计学意义(P<0.05)，常温无烫组各指标各时间点组内比较差异无统计学
意义(P>.05)。各指标同时间点组间比较差异有统计学意义(P<0.05)，
其变化幅度为高温烫伤组>呶挛尢套?Ｎ绿躺俗?Ｎ挛尢套椤?
(3)肺组织病理学变化
常温无烫组光镜下见肺泡大小均匀，肺泡隔大部分由1一2层细胞组
成，毛细血管轻度扩张，有少量炎性细胞浸润。常温烫伤组肺血管轻度
充血，肺泡隔增宽，可见少量中性粒细胞浸润，肺泡有不同程度萎陷而
大小不均。高温无烫组肺血管轻度扩张，内有红细胞浸润，偶见肺泡腔
内红细胞，肺泡隔中有炎性细胞浸润，部分肺泡融合。高温烫伤组肺血
管明显扩张充血，肺泡腔及肺间质充满大量的红细胞，肺泡隔明显增宽，
内有炎性细胞浸润，部分肺泡融合。
结论:(l)湿热环境下烫伤兔受湿热及烫伤双重因素的影响全身生理反
应加重，且全身生理反应与低氧血症的发生发展相一致;(2)湿热环境
下烫伤兔受高温及烫伤两种有害因素作用较早引起低氧血症，伤后80min
出现轻度低氧血症，且此时氧解离曲线便处于转折部，PaO:稍下降则明
显影响血液氧合，伤后12Omin达到中度低氧血症，即I型呼吸衰竭(单
纯低氧血症型);(3)湿热复合烫伤条件下早期低氧血症主要由vA/Q失
调及弥散功能障碍引起肺换气功能障碍所致，而通气功能代偿性增强;
(4)湿热复合烫伤条件下，肺损伤较单因素条件下加重，主要表现为血
管通透性增加引起的血细胞渗出及炎性细胞浸润，成为低氧血症发生的
病理基础;(5)建议湿热复合烫伤条件下严密监测呼吸功能的变化，除
监测生命体征变化外，应尽早行血气监测，早期发现低氧血症并行高浓
度氧疗。
Objective To explore the time and development of hypoxemia of rabbits with scald injury in hot and humid environment and analyse the cause and pathogenesis of hypoxemia. The study is to offer theoretical bases to establish the assessment criteria of hypoxemia on scald injury in the south battlefields and regions and lay experiments foundation of monitoring and treatment of respiratory function of scald patients in south battlefields and regions.
Methods 24 New Zealand male rabbits were divided into 4 groups randomly with equal numbers. Rabbits observed without scald in normal environment was designated as group cwwt, those with scald in normal environment as group cwts, those without scald in hot and humid environment as group gwwt and those with scald in hot and humid environment as group gwts. The dorsal skin of rabbits with scald were immersed in 95 ℃ water for 30s. This procedure produced a full thickness burn of 30% total body surface area (TBSA). The hot and humid environment condition was Tdb38℃ and relative humidity 65%?%; The normal environment was Tdb2?1 ℃ and relative humidity 55% ?5%. The exposure time of each group was 120 minutes. During the test, the basic vital body and blood-gas indexes were taken once per 40 minutes. The rabbits of each group were skilled at 120min and rem em*I cm lung to have histological assessment.
Results (1) Changes in vital signs : Tr , RF as well as HR of the rabbits in group gwts and group gwwt increased gradually during the experiment
(P<.05), MAP decreased gradually (P<.05); HR of the rabbits in group cwts increased gradually after scald (P<.05), MAP decreased gradually
(P<0.05), but Tr and RF had no changes during the experiment (P>.05); The indexes of vital signs of rabbits in group cwwt had no changes during the
-4-
experiment (P>0.05). Based on the comparison of inter-group at the same time, the width of the change of each index is that group gwts>group gwwt>group cwts>group cwwt (P<.05).
(2) Changes of blood gas: PaO2 of the rabbits in group gwts decreased in the SOmin period after scald (P<.05), SaO2 decreased in the 120min period (P<.05), PaCO2 decreased gradually and PA-aO2 increased gradually (P<.05). PaO2 and SaO2 of the rabbits in groups gwwt and cwts didn't change during the experiment (P>0.05), but PaCO2 decreased gradually and PA-aO2 increased gradually (P<.05). The indexes of blood gas of rabbits in group cwwt didn't change during the experiment (P>0.05). Based on the comparison of inter-group at the same time, the width of the change of each index is that group gwts>group gwwt>group cwts>group cwwt (P<.05).
(3) Histological changes of lung: Compared with the histological change in group cwwt, histological manifestation of damage to the lung occurred in group cwts gwwt gwts were characterized by the widening of alveolar wall with inflammatory cellular and red blood cell infiltration, the group gwts was more serious than the other groups.
Conclusion (1) The changes in vital signs of the rabbits with scald in hot and humid environment were more serious than that of each single factor. The changes were in accord with the development of hypoxemia; (2) The rabbits in the group gwts were injured mainly by hot and humid environment and scald with earlier hypoxemia, Obvious hypoxemia were observed at 80 minute after scald, at that tune the slight decrease of PaO2 may affect obviously SaO2. Hypoxemia after scald in hot and humid environment develops faster than that of scald in normal environment, it develops to type I respiratory failure at 120 minute after scald; (3) Hypoxemia after scald in hot and humid environment was caused by oxygenation failure resulting with VA/Q imbalance and disfunction of
-5-
diffusion capacity, with compensatory increasing of ventilatory function; (4) Histological damage to the lung after burn in hot and humid environment is more serious than that of burn in normal environment, it is characterized by the widening of alveolar wall with inflammatory cellular and red blood cell
方法：24只雄性新西兰兔随机分为常温无烫组(cwwt)、常温烫伤组(cwts)、高温无烫组(gwwt)和高温烫伤组(gwts)，每组6只。烫伤组动物背部及躯干两侧浸入95℃热水中30s制成30％Ⅲ度烫伤模型(Ⅲ度30％TBSA)，高温组的实验环境条件为Tdb(38±1)℃，Rh(65±5)％，常温组的实验环境条件为Tdb(24±1)℃，Rh(55±5)％。各组动物暴露时间均为120min，分别于伤前及伤后40min、80min、120min监测生命体征、动脉血气的变化，各组动物于120min处死，取肺组织做常规病理学检查。
结果：
(1) 生命体征的变化
高温无烫组和高温烫伤组动物施加干预条件后均出现Tr升高、RF和HR增快、MAP下降，各时间点组内比较差异有统计学意义(P＜0.05)；常温烫伤组烫伤后HR增快、MAP下降各时间点组内比较差异有统计学意义(P＜0.05)，但Tr、RF变化不明显，各时间点组内比较差异无统计学意义(P＞0.05)。常温无烫组各指标各时间点组内比较差异无统计学意义(P＞0.05)。各指标同时间点组间比较差异有统计学意义(P＜0.05)，其变化幅度为高温烫伤组＞高温无烫组＞常温烫伤组＞常温无烫组。
(2) 血气指标的变化
高温烫伤组PaO_2 80min开始下降，SaO_2 120min出现下降，与伤前比较差异有统计学意义(P＜0.05)，PA-aO_2和PaCO_2逐渐下降，各时间点组内比较差异有统计学意义(P＜0.05)，高温无烫组和常温烫伤组实验过
程中Pao:、SaO:变化不明显，各时间点组内比较差异无统计学意义
(P>0.05)，但PaCo:逐渐下降，PA一ao:逐渐升高，与伤前比较差异有统
计学意义(P<0.05)，常温无烫组各指标各时间点组内比较差异无统计学
意义(P>.05)。各指标同时间点组间比较差异有统计学意义(P<0.05)，
其变化幅度为高温烫伤组>呶挛尢套?Ｎ绿躺俗?Ｎ挛尢套椤?
(3)肺组织病理学变化
常温无烫组光镜下见肺泡大小均匀，肺泡隔大部分由1一2层细胞组
成，毛细血管轻度扩张，有少量炎性细胞浸润。常温烫伤组肺血管轻度
充血，肺泡隔增宽，可见少量中性粒细胞浸润，肺泡有不同程度萎陷而
大小不均。高温无烫组肺血管轻度扩张，内有红细胞浸润，偶见肺泡腔
内红细胞，肺泡隔中有炎性细胞浸润，部分肺泡融合。高温烫伤组肺血
管明显扩张充血，肺泡腔及肺间质充满大量的红细胞，肺泡隔明显增宽，
内有炎性细胞浸润，部分肺泡融合。
结论:(l)湿热环境下烫伤兔受湿热及烫伤双重因素的影响全身生理反
应加重，且全身生理反应与低氧血症的发生发展相一致;(2)湿热环境
下烫伤兔受高温及烫伤两种有害因素作用较早引起低氧血症，伤后80min
出现轻度低氧血症，且此时氧解离曲线便处于转折部，PaO:稍下降则明
显影响血液氧合，伤后12Omin达到中度低氧血症，即I型呼吸衰竭(单
纯低氧血症型);(3)湿热复合烫伤条件下早期低氧血症主要由vA/Q失
调及弥散功能障碍引起肺换气功能障碍所致，而通气功能代偿性增强;
(4)湿热复合烫伤条件下，肺损伤较单因素条件下加重，主要表现为血
管通透性增加引起的血细胞渗出及炎性细胞浸润，成为低氧血症发生的
病理基础;(5)建议湿热复合烫伤条件下严密监测呼吸功能的变化，除
监测生命体征变化外，应尽早行血气监测，早期发现低氧血症并行高浓
度氧疗。
Objective To explore the time and development of hypoxemia of rabbits with scald injury in hot and humid environment and analyse the cause and pathogenesis of hypoxemia. The study is to offer theoretical bases to establish the assessment criteria of hypoxemia on scald injury in the south battlefields and regions and lay experiments foundation of monitoring and treatment of respiratory function of scald patients in south battlefields and regions.
Methods 24 New Zealand male rabbits were divided into 4 groups randomly with equal numbers. Rabbits observed without scald in normal environment was designated as group cwwt, those with scald in normal environment as group cwts, those without scald in hot and humid environment as group gwwt and those with scald in hot and humid environment as group gwts. The dorsal skin of rabbits with scald were immersed in 95 ℃ water for 30s. This procedure produced a full thickness burn of 30% total body surface area (TBSA). The hot and humid environment condition was Tdb38℃ and relative humidity 65%?%; The normal environment was Tdb2?1 ℃ and relative humidity 55% ?5%. The exposure time of each group was 120 minutes. During the test, the basic vital body and blood-gas indexes were taken once per 40 minutes. The rabbits of each group were skilled at 120min and rem em*I cm lung to have histological assessment.
Results (1) Changes in vital signs : Tr , RF as well as HR of the rabbits in group gwts and group gwwt increased gradually during the experiment
(P<.05), MAP decreased gradually (P<.05); HR of the rabbits in group cwts increased gradually after scald (P<.05), MAP decreased gradually
(P<0.05), but Tr and RF had no changes during the experiment (P>.05); The indexes of vital signs of rabbits in group cwwt had no changes during the
-4-
experiment (P>0.05). Based on the comparison of inter-group at the same time, the width of the change of each index is that group gwts>group gwwt>group cwts>group cwwt (P<.05).
(2) Changes of blood gas: PaO2 of the rabbits in group gwts decreased in the SOmin period after scald (P<.05), SaO2 decreased in the 120min period (P<.05), PaCO2 decreased gradually and PA-aO2 increased gradually (P<.05). PaO2 and SaO2 of the rabbits in groups gwwt and cwts didn't change during the experiment (P>0.05), but PaCO2 decreased gradually and PA-aO2 increased gradually (P<.05). The indexes of blood gas of rabbits in group cwwt didn't change during the experiment (P>0.05). Based on the comparison of inter-group at the same time, the width of the change of each index is that group gwts>group gwwt>group cwts>group cwwt (P<.05).
(3) Histological changes of lung: Compared with the histological change in group cwwt, histological manifestation of damage to the lung occurred in group cwts gwwt gwts were characterized by the widening of alveolar wall with inflammatory cellular and red blood cell infiltration, the group gwts was more serious than the other groups.
Conclusion (1) The changes in vital signs of the rabbits with scald in hot and humid environment were more serious than that of each single factor. The changes were in accord with the development of hypoxemia; (2) The rabbits in the group gwts were injured mainly by hot and humid environment and scald with earlier hypoxemia, Obvious hypoxemia were observed at 80 minute after scald, at that tune the slight decrease of PaO2 may affect obviously SaO2. Hypoxemia after scald in hot and humid environment develops faster than that of scald in normal environment, it develops to type I respiratory failure at 120 minute after scald; (3) Hypoxemia after scald in hot and humid environment was caused by oxygenation failure resulting with VA/Q imbalance and disfunction of
-5-
diffusion capacity, with compensatory increasing of ventilatory function; (4) Histological damage to the lung after burn in hot and humid environment is more serious than that of burn in normal environment, it is characterized by the widening of alveolar wall with inflammatory cellular and red blood cell
引文
1．王正国主编．创伤外科学．上海：上海科学技术出版社，2002，499．
2. Tripathi FM, Pandey K, Paul PS, et al. Blood gas studies in thermal bums. Burns, 1983,10(1):13-6.
3．李国辉．40例烧伤病人的血气分析．中华整形烧伤外科杂志，1987，3(2)：124．
4．付琼芳，王旭．25例严重烧伤的早期血气分析．中华整形烧伤外科杂志，1987，3(4)：268-270．
5．陆增祺．军事医学词典．上海：上海辞书出版社，1997，162．
6．裴国献．重视热带地区战创伤救治研究．解放军医学杂志，2003，28(4)：285-288
7. Hayat H, Friedberg L. Heat-induced alterations in cell membrane permeability and inactivation of transformed mouse fibroblasts. Int J Hyperthermia, 1986, 2(4):369.
8. Russell GB, Graybal JM. Hypoxemic episodes of patients in a postanesthesia care unit. Chest, 1993,104(3):899-933.
9. Canet J, Ricos M, Vidal F. Early postoperative arterial oxygen desaturation. Anesth Analg, 1989,69(2):207-12.
10．钱桂生．低氧血症的原因与鉴别．中华实用内科杂志，2001，21(3)：130-131．
11．董声焕．呼吸衰竭基础与临床，北京：人民军医出版社，1992，89-90．
12. Anthonisen NR. Hypoxemia and O_2 therapy. Am Rev Respir Dis, 1982,126:729.
13. Pruitt BA, Flemma RJ, Divincenti FC, et al. Pulmonary complication in bum patients. The Journal of Thoracic and Cardiovasular Surgery, 1970, 59(1):7-20.
14. Miles D, Hurst TS, Saxena A. Systemic thermal injury in anesthetized rabbits causes early pulmonary vascular injury that is not ablated by lazaroids. Can J Anaesth, 1999 Feb;46(2):142-7.
15. Jin LJ, Lalonde C, Demling RH. Lung dysfunction after thermal injury in relation to prostanoid and oxygen radical release. J Appl Physiol, 1986, 61(1):103-12.
16. Demling RH, Lalonde C. Early postburn lipid peroxidation (effect of ibuprofen and allopuriol). Surgery, 1990,107(1):88.
17. Till GO, et al. Oxygen radical dependent lung damage following thermal injury of rat skin. Trauma, 1983,23:269.
18．李洁英，汤青兰，严鸿才．大鼠严重烫伤早期肺组织超微结构变化．中华实验外科杂志，1990，7(2)：80-81．
19．李洁英，吴家云，汤青兰．大鼠严重烧伤对肺脏影响的研究．中华实验外科杂志，1985，2(3)：131-133．
20．罗慰慈主编．现代呼吸病学．北京：人民军医出版社，1997，34．
21．李继红，甘韶雨，朱国标等．热应激对血气及LPO、SOD等指标的影响．中华劳动卫生职业病杂志，1995，13(6)：345-346．
22．朱国标，辛火，李继红等．高热与皮质醇、泌乳素、LPO及SOD的关系．中国公共卫生学报，1994，13：218．
23．朱国标，李继红，李素华等．高温环境对细胞膜结构和功能的影响．解放军医学情报，1994，8(3)：142．
24. Holman ND, Schneider AJ. Multi-organ damages in exertional heat exposure stroke. Neth J Med, 1989, 35:38.
25．朱国标，甘韶雨，张克俊．热暴露对兔肺细胞膜结构的影响．中华劳动卫生职业病杂志，1995，13(1)：9-11．
26．邹飞，罗炳德．部队中暑防治手册．北京：军事医学科学出版社，2000．56．
27．刘亚玲，林树新，徐明达等．兔烫伤早期多器官功能模型的制备．第四军医大学学报，2001，22(3)：246-248．
28. Kerr CG, Trappe TA, Starling RD, et al .Hyperthermia during Olympic triathlon: influence of body heat storage during the swimming stage. Med Sci Sports Exerc, 1998, 30(1): 99-104.
28．朱光法，钮善福，孙波等．肺表面活性物质治疗急性呼吸窘迫综合征的实验研究．中国危重病急救医学，1998，10(9)：516-518．
29．邱仞之．环境高温与热损伤．北京：军事医学科学出版社，2000，557-566．
30．马德选，徐如祥，朱红胜．湿热环境对颅脑火器伤早期生命体征和病死率的影响．解放军医学杂志，2002，27(2)：147-149．
31. Tripathi FM, Pandey K, Paul PS, et al. Respiratory functions in thermal bums. Bums Incl Therm Inj, 1983,9(6):401-8.
32．黎鳌主编．烧伤治疗学．第二版．北京：人民卫生出版社，1995，84-86．
33. Cathiram P, Caffin SL, Brock-Utne JG, et al. Prophycitc corticostevoid suppresses endotoxemia in heat-stressed primates. Aviat space Environ Med, 1988,59(2):142.
34. Cathiram P, Caffin SL, Brock-Ume JG, et al.Time Course of endotoxemia and cardivasculor changes in heat-stressed primates. Aviat space Environ Med, 1987, 58(11):1071.
35．茅志成，邬堂春主编．现代中暑诊断治疗学．北京：人民军医出版社，2000，43-65．
36．蒋建新，栗永萍，黄跃生等．严重创伤后早期全身性损害基础研究的现状与展望．中华创伤杂志，2002，18(4)：197-199．
37．俞森洋主编．现代呼吸治疗学．北京：科学技术文献出版社，2003，72．
38．关魁，陈茵．严重烧伤后血气变化与酸碱平衡紊乱．中华烧伤创疡杂志，2002，14(2)：89-91．
39. Henig NR, Pierson DJ. Mechanisms of hypoxemia. Respir Care Clin N Am, 2000,6(4):501-21.
40．王迪浔主编．病理生理学．第四版．北京：人民军医出版社，1995，179-186．
41. Shapiro BA. Clinical application of blood gases. 3rd ed. INC Chicago: Year Book Medical publishers, 1982,72.
42．张镜如主编．生理学．第四版．北京：人民卫生出版社，1996，163-164．
43. Hemdon DN, Thompson PB, Traber DL. Pulmonary injury in burned patients. Crit Care Clin, 1985,1(1):79-96.
44. Bargues L. The lung of the thermally injured patient Rev Prat, 2002,
52(20):2253-7.
45. Hess D. Detection and monitoring of hypoxemia and oxygen therapy. Respir Care, 2000,45(1):65-80.
46．陈萍，赵海涛．氧疗．中国实用内科杂志，2001，21(3)：137-139．
2. Tripathi FM, Pandey K, Paul PS, et al. Blood gas studies in thermal bums. Burns, 1983,10(1):13-6.
3．李国辉．40例烧伤病人的血气分析．中华整形烧伤外科杂志，1987，3(2)：124．
4．付琼芳，王旭．25例严重烧伤的早期血气分析．中华整形烧伤外科杂志，1987，3(4)：268-270．
5．陆增祺．军事医学词典．上海：上海辞书出版社，1997，162．
6．裴国献．重视热带地区战创伤救治研究．解放军医学杂志，2003，28(4)：285-288
7. Hayat H, Friedberg L. Heat-induced alterations in cell membrane permeability and inactivation of transformed mouse fibroblasts. Int J Hyperthermia, 1986, 2(4):369.
8. Russell GB, Graybal JM. Hypoxemic episodes of patients in a postanesthesia care unit. Chest, 1993,104(3):899-933.
9. Canet J, Ricos M, Vidal F. Early postoperative arterial oxygen desaturation. Anesth Analg, 1989,69(2):207-12.
10．钱桂生．低氧血症的原因与鉴别．中华实用内科杂志，2001，21(3)：130-131．
11．董声焕．呼吸衰竭基础与临床，北京：人民军医出版社，1992，89-90．
12. Anthonisen NR. Hypoxemia and O_2 therapy. Am Rev Respir Dis, 1982,126:729.
13. Pruitt BA, Flemma RJ, Divincenti FC, et al. Pulmonary complication in bum patients. The Journal of Thoracic and Cardiovasular Surgery, 1970, 59(1):7-20.
14. Miles D, Hurst TS, Saxena A. Systemic thermal injury in anesthetized rabbits causes early pulmonary vascular injury that is not ablated by lazaroids. Can J Anaesth, 1999 Feb;46(2):142-7.
15. Jin LJ, Lalonde C, Demling RH. Lung dysfunction after thermal injury in relation to prostanoid and oxygen radical release. J Appl Physiol, 1986, 61(1):103-12.
16. Demling RH, Lalonde C. Early postburn lipid peroxidation (effect of ibuprofen and allopuriol). Surgery, 1990,107(1):88.
17. Till GO, et al. Oxygen radical dependent lung damage following thermal injury of rat skin. Trauma, 1983,23:269.
18．李洁英，汤青兰，严鸿才．大鼠严重烫伤早期肺组织超微结构变化．中华实验外科杂志，1990，7(2)：80-81．
19．李洁英，吴家云，汤青兰．大鼠严重烧伤对肺脏影响的研究．中华实验外科杂志，1985，2(3)：131-133．
20．罗慰慈主编．现代呼吸病学．北京：人民军医出版社，1997，34．
21．李继红，甘韶雨，朱国标等．热应激对血气及LPO、SOD等指标的影响．中华劳动卫生职业病杂志，1995，13(6)：345-346．
22．朱国标，辛火，李继红等．高热与皮质醇、泌乳素、LPO及SOD的关系．中国公共卫生学报，1994，13：218．
23．朱国标，李继红，李素华等．高温环境对细胞膜结构和功能的影响．解放军医学情报，1994，8(3)：142．
24. Holman ND, Schneider AJ. Multi-organ damages in exertional heat exposure stroke. Neth J Med, 1989, 35:38.
25．朱国标，甘韶雨，张克俊．热暴露对兔肺细胞膜结构的影响．中华劳动卫生职业病杂志，1995，13(1)：9-11．
26．邹飞，罗炳德．部队中暑防治手册．北京：军事医学科学出版社，2000．56．
27．刘亚玲，林树新，徐明达等．兔烫伤早期多器官功能模型的制备．第四军医大学学报，2001，22(3)：246-248．
28. Kerr CG, Trappe TA, Starling RD, et al .Hyperthermia during Olympic triathlon: influence of body heat storage during the swimming stage. Med Sci Sports Exerc, 1998, 30(1): 99-104.
28．朱光法，钮善福，孙波等．肺表面活性物质治疗急性呼吸窘迫综合征的实验研究．中国危重病急救医学，1998，10(9)：516-518．
29．邱仞之．环境高温与热损伤．北京：军事医学科学出版社，2000，557-566．
30．马德选，徐如祥，朱红胜．湿热环境对颅脑火器伤早期生命体征和病死率的影响．解放军医学杂志，2002，27(2)：147-149．
31. Tripathi FM, Pandey K, Paul PS, et al. Respiratory functions in thermal bums. Bums Incl Therm Inj, 1983,9(6):401-8.
32．黎鳌主编．烧伤治疗学．第二版．北京：人民卫生出版社，1995，84-86．
33. Cathiram P, Caffin SL, Brock-Utne JG, et al. Prophycitc corticostevoid suppresses endotoxemia in heat-stressed primates. Aviat space Environ Med, 1988,59(2):142.
34. Cathiram P, Caffin SL, Brock-Ume JG, et al.Time Course of endotoxemia and cardivasculor changes in heat-stressed primates. Aviat space Environ Med, 1987, 58(11):1071.
35．茅志成，邬堂春主编．现代中暑诊断治疗学．北京：人民军医出版社，2000，43-65．
36．蒋建新，栗永萍，黄跃生等．严重创伤后早期全身性损害基础研究的现状与展望．中华创伤杂志，2002，18(4)：197-199．
37．俞森洋主编．现代呼吸治疗学．北京：科学技术文献出版社，2003，72．
38．关魁，陈茵．严重烧伤后血气变化与酸碱平衡紊乱．中华烧伤创疡杂志，2002，14(2)：89-91．
39. Henig NR, Pierson DJ. Mechanisms of hypoxemia. Respir Care Clin N Am, 2000,6(4):501-21.
40．王迪浔主编．病理生理学．第四版．北京：人民军医出版社，1995，179-186．
41. Shapiro BA. Clinical application of blood gases. 3rd ed. INC Chicago: Year Book Medical publishers, 1982,72.
42．张镜如主编．生理学．第四版．北京：人民卫生出版社，1996，163-164．
43. Hemdon DN, Thompson PB, Traber DL. Pulmonary injury in burned patients. Crit Care Clin, 1985,1(1):79-96.
44. Bargues L. The lung of the thermally injured patient Rev Prat, 2002,
52(20):2253-7.
45. Hess D. Detection and monitoring of hypoxemia and oxygen therapy. Respir Care, 2000,45(1):65-80.
46．陈萍，赵海涛．氧疗．中国实用内科杂志，2001，21(3)：137-139．