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.

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), 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.

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

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

The canine model to study inhalaton injury established in our lab was employed,and neutrophil NADPH oxidase activity,blood gas analysis,lung water volume,chest radiographs,and pulmonary histopathological changes were observed in the dogs after they were exposed to smoke inhalaton.It was found that carbon monoxide poisoning,hypoxemia,metabolic aci-dosisi respiratory alkalosis and lung damage developed rapidly and early after smoke inhalation;white blood cells disappeared from the circulation 5 minutes after injury onward;the activity of neutrophil NADPH oxidase increased gradually from the 30th minute to the 6th hour after injury,then decreased and approached to its preinjury level in the 12th hour after injury.It is postulated on the basis of the above findings that neutrophils would accumulate in the lungs after smoke inhalation and experince a "respiratory burst" characterized by the activation of NADPH oxidase and the production of large amounts of oxygen and other active oxygen radicals,which would play a significant role in the pathogenesis of acute lung damage in the early stage of smoke inhalation injury.

Forty-one burn patients were divided into inhalation injury and non-inhalation injury groups.It was found that in the inhalation injury group,TXB2 level and TXB2/G-keto-PGF1? ratio in plasma and lung tissue were significantly elevated,circulatory platelet aggregate ratio markedly decreased,and blood viscosity greatly increased.Histopathologically,congestion,edema,hemorrhage and thrombosis were seen in lung tissue.The changes of TXB2 level and TXB2/6-keto-PGF1?ratio were parallel to the clinical course of the development of respiratory failure in the patients with body surface burns complicated with inhalation injury.It is believed that the imbalance of TXA2/PGI2 is one of the factors of respiratory failure in severe body surface burns complicated with inhalation injury.

Fifty percent TBSA third degree burns was inflicted to 24 dogs and they were treated with immediate fluid infusion (8 dogs),delayed conventional infusion (n=8),and delayed fast infusion (n=8),It was found that in the immediate and delayed fast infusiong groups,strike volume,strike index, left ventricular strike work index,right ventricular strike index and femoral arterial pressure were maintained at a level more than 50% of the normal and were gradually restored.Their pulmonary artery wedge pressure was larger than 1.3 kPa.ALT and LDH were increased but never exceeded the preburn level.DB,TB,UN,Cr,PaO2,P(A-a)O2 were maintained in the normal range.MDA RCR,ADP/O,ATP,positive blood culture rate,mortality rate and morbility of multiple organ failure were all lower than those of the delayed conventional infusion group.It is believed that in the early stage of burn injury,the development of multiple organ failure can prevented effectively with immediate infusion and partially with delayed fast infusion while delayed conventional infusion exerts no protection at all.