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

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.

To explore the role of apoptosis, apoptosis regulating genes in the pathogenesis and development of smoke inhalation injury. With smoke inhalation injury rat model, the changes int the expression of Bcl 2, Bax, Fas, FasL genes mRNA and protein contents and their relationship with apoptosis of lung tissue cells at different time points after the injury were observed with TUNEL, immunohistochemistry and RT PCR techniques. The results showed that: ①apoptosis indet of lung colls after smoke inhalation injury increased, ②expressions of Bcl 2, Bax, Fas, FasL genes were obviously up regulated in injury group, peaking at the 12th hour, whereas the peak of protein expression was at the 24th hour. Furthermore, a significant correlation was found between the expression of Fas, Fasl, Bax gene and apoptosis indices in lung cells. The results suggested that apoptosis participated in the early pathological process of smoke inhalation injury, and apoptosis regulating genes foot part in the regulation of apoptosis in smoke inhalation injury.

AIM: To study the effects of nitric oxide (NO) on mitochondrial damage caused by exogenous calcium. METHODS: Normal myocardial mitochondria were divided into three groups; L- arginine control group (CG), Ca2 + - damaged group (DG) and L - NAME - preserved group (PG). Mitochondria of all groups were incubated at 30℃ with reaction medium containing 20μmol/L EDTA, 100μmol/L CaC12 and 1 μmol/L L- NAME with 100μmol/L CaCl2 respectively. Then the NO2-/NO3- contents, mitochondrial viability and membrane potential were investigated. RESULTS: The NO2-/NO3 contents of DG was obviously higher than that of CG and PG, meanwhile, there was no obvious difference between CG and PG. Mitochondrial viability and membrane potential of DG were significantly lower than that of CG and PG, and negatively related to NO2-/NO3- contents ( r = - 0.5297, P < 0.01; r = -0.6041, P < 0.01 ). But, the mitochondrial viability and membrane potential of PG were still lower than that of CG. CONCLUSION: Exogenous calcium could activate mitochondrial nitric oxide synthase resulting in NO production and the latter play an important role in decreasing mitochondrial viability and membrane potential.

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.

AIM: To study the effects of nitric oxide (NO) on mitochondrial damage caused by exogenous calcium. METHODS: Normal myocardial mitochondria were divided into three groups; L-arginine control group (CG), Ca 2+-damaged group (DG) and L-NAME-preserved group (PG). Mitochondria of all groups were incubated at 30℃ with reaction medium containing 20 ?mol/L EDTA, 100 ?mol/L CaCl 2 and 1 ?mol/L L-NAME with 100 ?mol/L CaCl 2 respectively. Then the NO- 2/NO- 3 contents, mitochondrial viability and membrane potential were investigated.RESULTS: The NO- 2/NO- 3 contents of DG was obviously higher than that of CG and PG, meanwhile, there was no obvious difference between CG and PG. Mitochondrial viability and membrane potential of DG were significantly lower than that of CG and PG, and negatively related to NO- 2/NO- 3 contents (r=-0.5297, P

AIM: To investigate the changes of gene expression of vascular endothelial growth factor(VEGF) in norepinephrine/ burn serum-induced astrocytes.METHODS: Immunofluorescence staining was used to show the distribution of VEGF in astrocytes after 24 h using norepinephrine/burn serum stimulation.Western blotting was used to detect protein expression of VEGF.Real time PCR was used to investigate expression of VEGF mRNA.RESULTS: ① Green fluorescence of protein expression of VEGF in astrocytes was increased when treated with high dose norepinephrine(50 ?mol/L).Green fluorescence of protein expression of VEGF in astrocytes was increased distinctness after burn serum stimulation.Green fluorescence protein expression of VEGF in astrocytes was increased significantly when high dose norepinephrine combined with burn serum stimulation was added.② VEGF protein expression in burn serum stimulating group was increased,and VEGF protein expression was significantly increased when burn serum was added during moderate(20 ?mol/L),high dose norepinephrine stimulation.③ Expression of VEGF mRNA was increased in burn serumtreated astrocytes.Expression of VEGF mRNA was increased significantly when norepinephrine-stimulated astrocytes exposed to barn serum,and as norepinephrine dose increases gradually.CONCLUSION: Norepinephrine and burn serum play an important role in inducing VEGF protein expression in astrocytes,suggesting that stress reaction of postburn is an important cause in inducing brain edema by excreting VEGF in astrocytes.

Objective To investigate effects of the complex therapy on severe inhalation injury. Methods The cases with inhalation injury and acute respiratory failure (ARF) of 4172 consecutive burn patients from Jan. 2000 to Feb. 2003 in our institute were studied retrospectively. Results 30 of the 128 patients with inhalation injury occurred acute ARF. 48 hours after the exogenous pulmonary surfactant (PS) was used to treat 6 cases with uncomplicated ARF, pulmonary function obviously ameliorated as compared with routine therapy. PaO 2 /FiO 2 rose from 239?33 mmHg to 317?28 mmHg(P

Objective To explore a suitable plan for the delayed rapid fluid resuscitation in burn patients with shock. Methods 20 patients with total body surface area (TBSA) burned over 40% admitted 4～8h after postburn were enrolled in this study. The patients were randomly divided into plasma and gelofusin groups. Rapid fluid replacement was given immediately after admission under close hemodynamic monitoring. Hemodynamic (PAP, PAWP, CO, PVR, SVR) and hemorrheological parameters, tissue oxygenation (DO 2, VO 2, O 2ext , lactic acid, base deficit) as well as indices reflecting the main visceral functions and damage were investigated. Results The amount of rapid fluid infusion within 2h after admission accounted for 38 8?6 1% of the amount calculated with the formula for the first 24h. When the infusion amount of pre-hospitalization was added, the amount would be (48 3?5 0)% of the amount for the first 24h. The real amount of the infusion for the first 24h was (31 4?14 3)% more than that of the amount calculated with the Evans formula. The real infused fluid amount for the second 24h was almost equal to the amount calculated with the formula. After fast fluid replacement therapy, all the parameters determined were markedly improved. Conclusions It is proposed that the formula for the delayed rapid fluid resuscitation in burn patients with shock should be: the amount infused for the first 24h (ml) =TBSA (%)?body weight (kg)?2 6,the ratio of colloid to electrolytes is 1:1, water=2000ml. Half of the total amount should be infused in the first 2h after admission under close hemodynamic monitoring. The amount infused for the second 24h (ml)=TBSA (%)?body weight (kg)?1,the ratio of colloid to electrolytes is 1:1, water=2000m1.

To clone the full length cDNA sequence of a novel expression sequence tag ST55 (GenBank Accession No. BI121646) from human umbilical vein endothelial cells stimulated by lipopolysaccharide, rapid amplification of cDNA ends (RACE) was used to extend the 3′and 5′ends of ST55 to obtain the full length cDNA sequence according to the known ST55 sequence. The cDNA was identified by Northern blot and analyzed with bioinformatics. A novel human full length cDNA was cloned and named endothelial overexpressed lipopolysaccharide associated factor 1( EOLA1 ) (GenBank Accession No. AY074889). This gene was located at chromosomal Xq27.3 and encodes a protein EOLA1 composed of 158 amino acids. Our data show that EOLA1 is a novel human gene associated with activated endothelial cells, and may play a role in intercellular signal transduction.