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Chinese burn medicine began in the " Great Leap Forward" movement, with the mark of the successful rescue of Qiu Caikang in Guangci Hospital (now known as Ruijin Hospital Affiliated to the Medical School of Shanghai Jiao Tong University), Shanghai. With the fading of the " Great Leap Forward" movement in 1962, medical staff of some burn bases such as Southwest Hospital of the Seventh Military Medical University (now known as the First Affiliated Hospital of Army Medical University) made a comprehensive summary on burn treatment, forming a set of original effective treatment protocols, which led to the improvement of burn treatment level. The stamp-like auto-allo intermingled skin grafting was created during that period, followed by the creation of an approach called " to embed small pieces of autogenic skin into the holes of a large sheet of allogenic skin" in Guangci Hospital, Shanghai. Owing to these approaches, the eschar of extensive burns was excised in multiple times, which led to the improvement of the cure level for extensive deep burn. Since then, the cure rate of burns of China continued to be the first in the world. Unfortunately, with the beginning of the " Great Cultural Revolution" , the development of Chinese burn medicine was interrupted and stopped. With the founding of the " Revolutionary Committee" in 1969, the Chinese burn medicine just started to recover. After 1978, the Chinese burn medicine began to rise rapidly again. Since then, the theoretic research on burns has been conducted in China, just as a follower at the beginning, and then as a runner in 1990s′, but as a leader in 2000s′ in some fields such as inhalation injury, sepsis, and wound healing, etc. At present, the clinical cure rate of burns in China is ranked in the leading position in the world, and the theoretical research on burns is also among the advanced ranks in the world.
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Objective To investigate the therapeutic effects of delayed lung lavage with exogenous pulmonary surfactant(PS)diluent on endogenous surfactant system dysfunction and acute respiratory failure caused by severe smoke inhalation in rats.Method Ninety Wistar rats were randomly separated into five groups:Group I,normal control(n=14);Group Ⅲ,smoke inhalation(n=27);GroupⅢ,smoke+PS lavage+mechanical ventilation(MV),n=21;Group IV,smoke+saline lavage+MV,n=10;Group V,smoke+MV,n=18.The lungs were lavaged with 30 ml/kg normal ssdine containing 100 mg/kg PS or same volume of saline via tra cheal catheter at 2 h after smoke inhalation,then the animals were placed on a ventilator for 4 h,and observed until 24 h after injury.The arterial blood gas level,lung water volume,static lung compliance(Cst),total protein and albumin contents in bronchoalveolar lavage fluid(BALF),surface tension properties of BALF,and fatality rate at 24 h were measured.Results Smoke inhalation caused a similar acute hypoxia and severe carbon monoxide poisoning immediately in all injured groups.The animals in group Ⅱ showed acute respiratory failure,serious hish permeability pulrnonary edema,and surfactant system dysfunction.The surface tension properties of BALF and Cst were significantly improved by delayed lung lavage treated with exogenous PS diluent in group m(P<0.05).However,the lung water volume,total protein and albumin contents in BALF and the oxygenation had not significant difference between group Ⅲ and group Ⅱ(P>0.05).Conclusions Delayed lung lavage with exogenous PS diluent,at a certain extemt,restored endogenous suffactant function inhibited by smoke inhalation and improved lung function.Nevertheless,the trent could not alleviate rash permeability pulmonary edema and respiratory failure drarnatically.The expected decrease of mortality at early stage after smoke inhalation injury was not showed yet.
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Objective To investigate the effects of NF-κB activation on paihogenesis of PMN aggregation in myocardium and early myocardial dysfunction induced by polymorphonuclear leukocyte (PMN) in burned rats. Method One hundred and seventy wistar rats were randomly divided into three groups, control group ( n = 20, with isotonic saline solution), bum group ( n = 90, with isotonic saline solution after bum), bum and pyrrolidine dithioncarbamate group ( PDTC group, n = 60, with isotonic saline solution and 250 mg/kg PDTC after bum). The rats in bum group and PDTC group underwent 35% TBSA full-thickness bums on the back. The acb'vaty of myocardial NF-κB was tested by electrophoretic mobility shift assay (EMSA) at 1, 3, 6, 12,24 postbum hours (PBH). Expressions of myocardial IL-8 and ICAM-1 mRNA were assessed by reverse transcription polymerase chain reaction (RT-PCR) at 3,6,12,24 PBH. Meanwhile, the avtivity of myocardial myeloperoxidse(MPO), the left ventricular systolic pressure(LVSP) and the left ventricular end diastolic pressure (LVEDP) as well as maximum positive and negative left ventricular pressure change (± dp/dtmax) were observed at 3,6,12,24 PBH. Results The activity of myocardial NF-κB in bum groups was markedly increased at 1 PBH [(20.27± 3.43) × 104 A] .which was obviously higher than that in control group [(2.18±0.38) × 104 A, P < 0.01], and was still higher than that in control group at 24 PBH ( P < 0.01). The expressions of myocardial IL-8 and ICAM-1 mRNA and avtivity of myocardial myeloperoxidse were obviously higher than that in control group at 3,6,12,24 PBH respectively (P < 0.01), LVSP and ± dp/dtmax significantly were lower, but LVEDP was higher than that in control group during 3-24 PBH (P < 0.01). Compared with that in bum group, these indices were ameliorated in PDTC group. Conclusions Severe bum might activate myocardial NF-κB, which ultimately lead to the production of cytokines, PMN aggregation in myocardium and deterioration of cardiac contractility and relaxation consequently.
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Objective To investigate the effects of norepinephrine (NE) on vascular endothelial growth factor (VEGF) expression of brain tissues in severe burn rats. Methods The healthy male Wistar rats were made into 40%TBSAⅢ?burn models to observe the effect of NE on blood brain barrier. In the meantime, effect of NE was examined by means of immunocytochemistry and real time PCR. Results (1) Permeability of blood brain barrier was increased in burn and burn with NE stimulating rats, with significantly statistical difference compared with normal control group (P
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Objective To identify the promoter sequence of endothelial-overexpressed lipopolysaccharideassociated factor 1 ( EOLA1) gene and to elucidate the molecular mechanisms controlling EOLA1 expression. Methods A DNA fragment containing 1 723 bp 5' upstream of the EOLA1 gene and the transcription start site was generated by polymerase chain reaction and then cloned into a luciferase reporter gene vector,pGL3-basic. The relative luciferase activities driven by this 5'-upstream fragment and a series of deletion mutants were measured in transiently transfected human ECV304 cells,respectively. At last,the 1 723 bp upstream of the EOLA1 gene was analyzed online with Cluster Buster. Results A fragment 785 bp upstream of the EOLA1 coding region was sufficient to promote transcription. Further deletion analysis of the 785 bp fragment indicated that a 68 bp element from-738 to -676 was important for EOLA1 transcription in ECV304 cells. The 1 723 bp sequence contains binding sites for Sp1 and Myf. Conclusion We map the EOLA1 promoter by deletion analysis and reveal that the proximal region ( -738 to -676 bp) ,which contains binding sites for Sp1 and Myf,is essential for human EOLA1 promoter activity in ECV304 cells.
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Objective To investigate the effects of norepinephrine on brain edema of rats in 24 h after severe burn.Methods A total of 48 healthy Wistar rats were randomly divided into 8 groups: normal control group,1,2,5 mg/kg norepinephrine,burn group,burn with 1,2,5 mg/kg norepinephrine pretreatment groups(n=6 in each group).The rats in all burn groups were scalded into 40%TBSAⅢ degree burn.Pathological features were observed,and blood brain barrier,brain water(%) were examined in postburn 24 h.Results Pathological evidence of brain edema exhibited in the burn group and burn group with norepinephrine pretreatment,and increased permeability of blood brain barrier and brain water were observed.The burn with norepinephrine pretreatment groups were more significantly severe in comparison with simple burn groups and normal control group.Conclusion Norepinephrine may play an important role in brain edema in postburn 24 h,suggesting that stress of postburn may induce brain edema.
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Objective To investigate the changes of myocardial mitochondrial permeability transition pore(PTP) and its mechanism in the early stage after severe burns. Methods An experimental model of 30% TBSA full thickness skin scalding was established in rats. All rats were injected with deoxyglucose(DOG) before sacrifice. Myocardial mitochondrial DOG and cytochrome c content, Ca 2+ concentration([Ca 2+ ] m) and MDA content were determined. Results ① There were no obvious changes of mitochondrial DOG and cytochrome c content at 1 h after burns, but mitochondrial DOG increased evidently at 3, 6, 12 and 24 h after burns. Meanwhile, cytochrome c content was significantly lower than that of the control, being 68.8%, 50.0%, 77.1% and 72.9% of that in the control, respectively. ② [Ca 2+ ] m and MDA content were significantly higher than those of the control at 3, 6, 12 and 24 h after burns. ③ Mitochondrial DOG content was positively correlated with [Ca 2+ ] m and MDA content, respectively, after burns. Conclusion There is no obvious change in myocardial mitochondrial permeability transition pore, but PTP opening increases markedly at 3, 6, 12 and 24 h after burns. Mitochondrial Ca 2+ overloading and increase in free radicals may be the cause leading to PTP opening.
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Objective To investigate the roles of the activated p38 kinase in cell injury by observation of the effects of hypoxia and burn serum on cardiomyocyte p38 kinase and JNK activation. Methods Phosphorylation of p38 kinase and JNK in primary cultured neonatal rat cardiomyocytes before and after hypoxia and burn serum was determined by Western blotting. Effects of pretreatment with SB203580 at the dose of 10 ?mol/L on the changes of phosphorylation of p38 kinase in cardiomyocytes, lactate dehydrogenase (LDH) activity, cell vitality and apoptosis were investigated, respectively. Results Exposure of rat neonatal cardiomyocytes to hypoxia and burn serum resulted in a rapid and long lasting activation of p38 kinase but no significant activation of JNK. SB203580(10 ?mol/l), a selective inhibitor of p38 kinase, could inhibit p38 kinase activation dramatically, decrease the LDH activity in culture media and cell apoptosis significantly and improve cell vitality. Conclusion In the two stress activated signal pathways of MAPKs family, p38 kinase pathway, but not JNK, is the major pathway activated by hypoxia and burn serum and participates in the cardiomyocyte injury.
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Objective To investigate the protective effects of diazoxide on cardiomyocytes after severe burn injury Methods A total of 24 healthy Wistar rats were randomized into normal control group(Control), burn group(Burn) and diazoxide treated group(Diazo)( n =8) Rats in Burn and Diazo groups were inflicted with 30%TBSA Ⅲ degree burn and resuscitated with Ringer's solution intraperitoneally 30 min after burn Diazoxide was injected into rats in Diazo group at the dose of 10 mg/kg through the external jugular vein After rats were sacrificed at 6 h after burn, myocardial mitochondrial K + influx, respiratory function, Ca 2+ concentration ([Ca 2+ ]m), MDA content, serum CK and LDH levels were determined Results Mitochondrial K + influx of Diazo group was evidently higher than that in Control and Burn group Mitochondrial respiratory control rate(RCR) and ST 3 in Diazo group were higher than that in Burn group However, [Ca 2+ ]m, MDA, CK and LDH levels in Diazo group were significantly lower than those in Burn group Conclusion Diazoxide can attenuate the damage to cardiomyocytes after severe burn injury, which might be related to the opening of mitochondrial K + channel, inhibition of mitochondria from Ca 2+ overloading and decrease of free radical production
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Objective To investigate the properties of the serum free binding of vascular endothelial cells(ECs) to lipopolysaccharide (LPS). Methods The binding of ECs to fluorescein isothiocyanate labelled LPS(FITC LPS) was observed with laser confocal microscope(LCM). The extract of ECs membrane after binding with FITC LPS was recorded with fluorescence microscope. Results The binding of ECs to FITC LPS was in a dose dependent manner. The fluorescence was mainly distributed in cytoplasm, especially near the nucleus which could also be stained. The bound FITC LPS had a very close relationship with the membranous system of ECs. Conclusion ECs could bind to LPS directly and could function intracellularly.
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Objective To investigate the changes of gastric mucosal blood flow and intramucosal pH value (pHi) during severe intraperitoneal infection in rats and the related significance. Methods The intraperitoneal infection rat model was established by cecal ligation and puncture (CLP). Laser Doppler blood flow meter on micro circulation and the vitreous electrode were used to examine the gastric mucosal blood flow and the gastric mucosal pH value, respectively. Results The gastric mucosal blood flow (GMBF) in the infected group was significantly lower than that in the control group ( P
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Objective To investigate the effects of cerebellum fastigial nucleus stimulation (FNS) on right middle cerebral artery occlusion (MCAO) rats with autonomic cardiovascular function disturbances. Methods MCAO model was employed in this study. A total of 60 MCAO rats were randomly divided into FNS group and non cerebellum fastigial nucleus stimulation group (NFNS). The time domain, power spectral components, and chaos of heart rate variability (HRV) were analyzed. Results The power spectral components and chaos of HRV at 3, 5, and 10 d after MCAO were significantly lower than those in the sham group ( P
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<p><b>OBJECTIVE</b>To explore the role of massive escharectomy at early postburn stage in the prevention of internal organ dysfunction.</p><p><b>METHODS</b>(1) Ten cases of severely burned patients were randomly divided into early (A) and non-early escharectomy (B) groups in equal number. Venous blood samples were harvested from the patients of the two groups in 1, 3 and 7 postburn days (PBDs), And the samples from 6 healthy volunteers were taken as the control. The serum was separated from the above blood samples and was employed to stimulate cultured HUVECs in vitro. The cell viability and permeability was observed after the stimulation. (2) Seventy Wistar rats inflicted with 30% TBSA III degree scalding were used as an animal model, and were randomized into early (C, n = 30) and non-early escharectomy (D, n = 30) groups, with 5 normal rats as control in each group. Intra-peritoneal fluid infusion was carried out at 1, 3, 6, 12, 24 and 48 postburn hours (PBHs) in rats in both groups. The rats were killed by blood letting at 1 hour after fluid supplementation. The changes in peritoneal macrophage (M Phi) activation state and plasma contents of LPS, IL-8, PLA(2) and MDA were determined at 48 hours after escharectomy in the rats.</p><p><b>RESULTS</b>The cell viability and permeability of the HUVECs co-cultured with the serum from burn patients in E group was much better preserved than that in B group. On the other hand, the peritoneal M Phi activation and the plasma contents of LPS, IL-8, PLA(2) and MDA in C group were obviously decreased compared with those in D group.</p><p><b>CONCLUSION</b>Early postburn escharectomy to remove denatured burned tissue were proved to be helpful in ameliorating endothelial injury and in inhibiting activation of inflammatory cells. Therefore, early escharectomy was assumed to be beneficial in the prevention of postburn SIRS and MODS.</p>
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Adulto , Animais , Feminino , Humanos , Masculino , Ratos , Queimaduras , Sangue , Cirurgia Geral , Divisão Celular , Linhagem Celular , Permeabilidade da Membrana Celular , Meios de Cultivo Condicionados , Química , Dinoprostona , Metabolismo , Endotélio Vascular , Biologia Celular , Interleucina-8 , Sangue , Lipopolissacarídeos , Sangue , Macrófagos Peritoneais , Metabolismo , Malondialdeído , Sangue , Insuficiência de Múltiplos Órgãos , Óxido Nítrico , Metabolismo , Fosfolipases A , Sangue , Metabolismo , Distribuição Aleatória , Ratos Wistar , Fatores de Tempo , Fator de Necrose Tumoral alfa , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the significance of the expression pattern and its signal modulating mechanism of endothelial ICAM-1 induced by LPS.</p><p><b>METHODS</b>(1) The expression pattern of the ICAM-1 was observed at mRNA level in cultured human umbilical vascular endothelial cells (HUVECs) strain ECV-304 after being stimulated by different LPS concentrations at different time points. (2) The modulating effects of different signal pathways on the ICAM-1 expression of the HUVECs were observed at mRNA and protein levels under the stimulation of LPS after the cells were primed by signal pathway blocking agents for 30 mins.</p><p><b>RESULTS</b>(1) The ICAM-1 mRNA expression could be induced by LPS (100 pg/ml) for 6 hours, and the expression was enhanced along with the increase of LPS concentration. The expression peaked when LPS was at concentrations of 100 approximately 1 000 ng/ml. Temporally, the mRNA expression reached the top level at 6 approximately 8 hours and remained high 12 hours after the stimulation. (2) The expressions of ICAM-1 mRNA and protein could be significantly inhibited by PSI, the NF-kappaB inhibitor. Moreover, the expression of ICAM-1 could all be partially inhibited at mRNA and protein levels by PD98059, the ERK1/2MAPK inhibitor, as well as SB203580, the p38MAPK inhibitor.</p><p><b>CONCLUSION</b>The ICAM-1 mRNA expression of HUVECs could be induced by LPS in both dose and time dependent manner. NF-kappaB might be the major signal pathway of modulating ICAM-1 expression, and p38 and ERK1/2 could possibly be signal pathways of minor importance.</p>
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Humanos , Células Cultivadas , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica , Molécula 1 de Adesão Intercelular , Genética , Lipopolissacarídeos , Toxicidade , Proteínas Quinases Ativadas por Mitógeno , Fisiologia , NF-kappa B , Fisiologia , Transdução de Sinais , Fatores de TempoRESUMO
<p><b>OBJECTIVE</b>To investigate relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats.</p><p><b>METHODS</b>Wistar rats inflicted by 40% TBSA III degree scalding were employed as the model. The myocardial tissue was obtained from the left ventricle at different postburn time points. Apoptosis was determined by the determination of myocardial tissue Caspase-3 activity and TUNEL staining (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling). The LVSP (left ventricular systolic pressure), LVEDP (left ventricular end-diastolic pressure) and +dp/dtmax (the rate of the rise of left ventricular pressure) and -dp/dtmax (the rate of the fall of left ventricular pressure) were all monitored by four-channel physiological recorder. In addition, myocardial activities of MPO and SOD were detected.</p><p><b>RESULTS</b>The TUNEL staining of rat myocardial cells was positive at 6 postburn hour (PBH) and reached top level at 12 PBH. The change in Caspase-3 activity was earlier than that of apoptotic morphology and reached peak values at 3 and 6 PBHs. The left ventricular function (systolic and diastolic function) was significantly impaired after the scalding and dropped to the lowest levels at 12 PBHs. The increase in myocardial tissue MPO activity was accompanied by the decrease in SOD activity.</p><p><b>CONCLUSION</b>Myocardial cellular apoptosis was one of the reasons of postburn myocardial injury in scalded rats. Caspase protease cascade pathway might be involved in the process of apoptosis, which suggested that the initiation of apoptosis was closely related to the infiltration of neutrophils and to the release of large amounts of oxygen free radicals in myocardial tissue.</p>
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Animais , Feminino , Masculino , Ratos , Apoptose , Queimaduras , Patologia , Caspase 3 , Caspases , Metabolismo , Miócitos Cardíacos , Patologia , Peroxidase , Metabolismo , Ratos Wistar , Superóxido Dismutase , Metabolismo , Função Ventricular EsquerdaRESUMO
<p><b>OBJECTIVE</b>To screen the optimal transfection method for human umbilical vein endothelium, so as for us to establish a basic method for the further transfection with other objective genes.</p><p><b>METHODS</b>The pEGFP-Actin plasmid was employed as an ectogenetic gene and was transfected into ECV-304 endothelium cells by lipofection, DEAE-dextran or electroporation transfection methods, respectively. The cell death rate and transfection rate after the transfection were compared among the three methods.</p><p><b>RESULTS</b>(1) Twelve hours after the transfection, the cell death rate was 4% by all three methods, however, the cell death rate increased up to 50% at 60 hours after the transfection by DEAE-dextran. (2) The transfection rate of ECV-304 could reach 95% by all the three methods. But the fluorescent intensity was stronger in lipofection group compared with electroporation method.</p><p><b>CONCLUSION</b>Gene transfection into ECV-304 with lipofection and electroporation methods exhibited better stability and repeatability.</p>
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Humanos , Actinas , Genética , Células Cultivadas , Eletroporação , Endotélio Vascular , Fisiologia , Vetores Genéticos , Genética , Plasmídeos , Genética , Proteínas Recombinantes de Fusão , Genética , Transfecção , MétodosRESUMO
<p><b>OBJECTIVE</b>To investigate the role of the change in glucocorticoid receptor in stress-induced gastric ulcer in severely burned rats.</p><p><b>METHODS</b>Wistar rats inflicted with 30% TBSA full-thickness burn were employed as the model. The dynamic postburn change in the glucocorticoid receptor in gastric mucosal tissue and gastric mucosal injury (injury index) were observed.</p><p><b>RESULTS</b>The gastric mucosal cortisol content increased as of 3 postburn hours (PBHs) and peaked at 12 PBHs. But the cytoplasmic glucocorticoid receptor content in the gastric mucosal cells decreased evidently. In addition, the gastric mucosal injury index increased obviously at 12 and 24 PBHs.</p><p><b>CONCLUSION</b>The decrease of gastric mucosal cytoplasmic glucocorticoid receptor content might be closely related to the stress-induced gastric mucosal injury.</p>
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Animais , Masculino , Ratos , Queimaduras , Metabolismo , Modelos Animais de Doenças , Ratos Wistar , Receptores de Glucocorticoides , Metabolismo , Fisiologia , Úlcera Gástrica , Metabolismo , Estresse FisiológicoRESUMO
<p><b>OBJECTIVE</b>To investigate the influence of N-acetyl-L-cysteine (NAC) on pulmonary injury and oxygen stress caused by smoke inhalation injury.</p><p><b>METHODS</b>Rats inflicted with smoke inhalation injury were employed as the model. WBC in BALF (bronchoalveolar lavage fluid), MPO (myeloperoxidase) activity, hydrogen peroxide (H(2)O(2)) content, GSH (glutathione) content and total antioxidant (TAO) capacity in pulmonary tissue were determined.</p><p><b>RESULTS</b>Postinjury WBC in BALF, MPO activity in pulmonary tissue and H(2)O(2) content decreased obviously after NAC treatment. But the pulmonary tissue contents of GSH and ATO increased evidently after the treatment with NAC.</p><p><b>CONCLUSION</b>NAC treatment could ameliorate pulmonary oxygen stress after smoke inhalation injury. AS a result, the pulmonary antioxidant capacity was improved.</p>
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Animais , Ratos , Acetilcisteína , Farmacologia , Líquido da Lavagem Broncoalveolar , Modelos Animais de Doenças , Sequestradores de Radicais Livres , Farmacologia , Glutationa , Metabolismo , Peróxido de Hidrogênio , Metabolismo , Leucócitos , Estresse Oxidativo , Peroxidase , Metabolismo , Ratos Wistar , Lesão por Inalação de Fumaça , Metabolismo , PatologiaRESUMO
<p><b>OBJECTIVE</b>To observe the rule of the change of apoptosis and proliferation of pulmonary tissue cells in rats with inhalation injury, so as to explore the significance of apoptosis in the repairing process of pulmonary tissue injury.</p><p><b>METHODS</b>Smoke inhalation injury model was established in rats. The rats were randomly divided into normal control (NC) and smoke inhalation injury (SI) groups. TUNEL and immunohistochemistry methods were employed to determine the changes in cellular apoptotic and proliferating cell nuclear antigen (PCNA) indices of the pulmonary tissue at different postburn time points.</p><p><b>RESULTS</b>(1) The apoptotic index increased at 2 postburn hours (PBHs) and remained at high levels thereafter. (2) The PCNA index increased at 12 PBHs, reaching top level at 3 postburn days (PBDs), remaining kept at relativly high level later.</p><p><b>CONCLUSION</b>Apoptosis not only played roles in the early pulmonary injury after smoke inhalation injury, but also participated in the repair and modification of the proliferated tissue during later reconstruction.</p>
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Animais , Feminino , Masculino , Ratos , Apoptose , Divisão Celular , Modelos Animais de Doenças , Pulmão , Patologia , Antígeno Nuclear de Célula em Proliferação , Metabolismo , Ratos Wistar , Lesão por Inalação de Fumaça , Metabolismo , PatologiaRESUMO
Objective To explore the feasibility and safety of massive lung lavage to dogs in the early stage after acute serious smoke inhalation. Methods A total of 16 dogs were inflicted with smoke inhaled injury and then divided into group A (n=5) without lung lavage, group B (n=6) in which left lung lavage was followed by lavage on the right 30 min later, and group C (n=5) in which the interval of the lavages on the left and right lung was 4 h. Massive lung lavage was carried out in 1 h after the injury under the guiding fiberoptic bronchoscopy and a special ventilation jet was served to supply enough oxygen to the dogs. The stability of pulmonary function and blood circulation were observed at different time points in every group. Results The average operating time of unilateral lung lavage was about 15 minuted and the liquid volume left in every lung after operation was from 100 ml to 140 ml when the total lavaging volume was kept in 250 ml. The changes of hemodynamic parameters were identical in Group B and Group C. Inhalation injury had certain negative effect while lung lavage almost had no effect on the blood circulation of the animals in 2 lavage groups. No serious cardiac arrythemia was found in them during the lavaging. Pulmonary function in Group C was better than that in Group B but worse than that in Group A. In the 2 lavaging groups, PaO2 remained higher than 9.33 kPa(FiO2=0.4)during and after the lavaging. Conclusion The ventilation mode and the lavage method introduced here ensure the safety of massive lung lavage in dogs with acute smoke serious inhalation injury.