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.

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

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.

Objective To construct small interfering RNA(siRNA) expression vectors targeting EOLA1 (Endothelial-overexpressed lipopolysaccharide-associated factor 1) gene, and to assay their effects on the expression of EOLA1. Methods GFP-EOLA1 fusion protein expressive vector pEGFP-N2/EOLA1 was constructed and transfected into ECV304 cells. The transfected cells were cultured in M199 containing G418 (400?g/ml) for 5 weeks to screen the cell line stably expressing GFP-EOLA1 fusion protein. For interfering EOLA1 target gene, complementary oligonucleotides were desiqned and synthesized at different sites. The oligonucleotides were inserted into pSinencer3.1/H1 plasmid. Then, the vector was transfected into the ECV304 cells stably expressing GFP-EOLA1 fusion protein and the inhibiting affection to target gene EOLA1 was identitied by the observation of the green fluorescence in transfected cells with inverted fluorescent microscope and Western immunoblot assay. Results The ECV304 cell line stably expressing GFP-EOLA1 fusion protein was constructed, and the siRNA vector of EOLA1 can knockdown EOLA1 gene expression specifically. Conclusion The siRNA vectors specifically interfering EOLA1 expression were constructed successfully, which would be useful in the study of function of EOLA1 gene.

Objective To screen and analyze genes up regulated in human umbilical vein endothelial cells (HUVEC) stimulated by lipopolysaccharide (LPS). Methods Suppression subtractive hybridization (SSH) was performed between the unstimulated HUVEC(driver) and HUVEC stimulated with LPS(tester) to generate subtractive cDNA library. The library was screened with colony dot hybridization to further verify the differentially expressed cDNA clones. Positive clones were sequenced and BLAST analyzed. The 3 novel cDNA sequences were verified by RT PCR. Results Twenty five up regulated genes related to inflammation, cellular cytoskeletal rearrangement, cellular proliferation and apoptosis, intercellular message transduction, and 3 new expression sequence tags (EST) were acquired. RT PCR indicated the expression of the new ESTs only in HUVEC stimulated by LPS. Conclusion SSH is a powerful technique of high sensitivity for the detection and clone of up regulated gene expressed in HUVEC stimulated by LPS, which may be helpful to clarify the mechanism of endothelial cells activation stimulated by LPS.

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.

The serial changes in thromboxane (TXA2) prostacyclin(PGI2),circulatory platelet aggregate ratio (CPAR),platelet count,blood viscosity,myocardial enzyme spectrum,cortisol and epinephrine were determined in 42 severely burnt patients randomly divided into two groups.The findings demonstrated that in the control group,both TXA2 and TXA2/PGI2 ratio increased significantly during the early postburn stage.Myocardial enzyme spectrum,blood viscosity,cortisol and epinephrine also increased markedly.However,levels of the above parameters in the anisodamine-treated group were significantly lower than in the control following the infusion of anisodamine.On the contrary,CPAR and platelet count in the treated group increased and were significantly higher than those in the control.Moreover,TXA2 was closely correlated with CPAR,platelet count,blood viscosity and myocardial enzyme spectrum (P