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.

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

Male Wistar rats were randomized into 3 groups:The rats of group I received sham burning to serve as the control and those of groups and Ⅲ were inflicted with 20% and 30% TBSA third degree phosphorus burns respectively.No treatment was given to group Ⅱ.Group Ⅲwas further divided into 2:The rats of subgroup Ⅰ were debrided immediately and those of subgroup Ⅱ in the 6th hour postburn.The findings were as follows;(l)The tissue content of phosphorus was more significantly decreased in subgroup Ⅰ than in subgroup Ⅱ-(2)Twenty-eight rats of subgroup Ⅰ all survived while 9 of the 44 rats of subgroup Ⅱ died with a mortality rate of 20.5%.The mortality rate of group Ⅱ was 37.5%(3/8).(3)The recovery of serum electrolytes and other biochemical parameters occurred earlier in subgroup I.Our findings suggest that debridement as early as possible after phosphorus burns contributes significantly to the decrease of the victims mortality.

Tamm-Horsfall protein(THP)was determined with radioimmunoassay in the urine and blood samples of 59 burn patients.It was found that urine and blood THP was significantly decreased postburn and the degree of decresing was correlated with the extent of the burnt body surface and the severity of renal damage.The changes of THP occurred earlier than those of the routine parameters for renal damage such as BUN or Cr.It is suggested that THP determination can be used as an index for the early damage of the Henle's loop and the distal convoluted tubules after burn injury.

Electrolyte imbslance.the changes of serum aldosterone and the ratio of an-giotensin Ⅱ/arterial natriuretic peptide were studied prospectiely in 59 cases of severe burns.Meanwhile,certain parameters of renal functions were detarmined.Hypernatremia devaloped in 6 cases.On the basis of our findings,it is believed that postburn hypernatremia might result from renal dysfunction and the greatly increased mediators,which can enhance the retention of sodium,might also play an important role in the development of postburn hypernatremia.

To elucidate apoptosis of polymorphonuclear leukocytes (PMN) in early postburn stage and the effects of burn sera and subeschar tissue fluid (STF) on apoptosis of PMNs, 24 Wistar rats were divided into scald group and control group (no scald group) randomly. PMNs were harvested at 0, 12, 24h after scald injury,and percentage of apoptotic PMNs was measured by flow cytometry.Apoptosis of PMNs was again assayed with flow cytometer after being incubated with burn sera or STF harvested from scalded rats. The result showed that the percentage of apoptotic PMNs in scalded group were lower than that in control group,indicating burn sera and STF could inhibit apoptosis of PMNs in a dose dependent manner. It suggested that spontaneous apoptosis of PMNs is inhibited in early postburn stage, and burn sera and STF play an important role in this process.

The aim of the study was to explore the role of NF ?B activation in the pathogenesis of smoke inhalation injury and to evaluate the effects of dexamethasone on NF ?B activation. 130 Wistar rats were inflicted with smoke inhalation injury and randomized equally into the control group, smoke inhalation injury group and dexamethasone treatment group.The expressions of NF ?B P 65 ,I?B ?,TNF ?,and ICAM 1 proteins in the lung tissue were determined by immunohistochemistry at 2,6,12,24,48,72 hours after smoke inhalation injury. The results showed that,after smoke inhalation ,the expressions of NF ?BP 65 ,TNF ?,and ICAM 1 increased,whereas the expression of I?B ? decreased. In the dexamethasone treatment group,the expressions of NF ?BP 65 ,TNF ?,and ICAM 1 were down regulated, and I?B ? was up regulated.These results suggest that NF ?B activation may participate in the pathogenesis of smoke inhalation injury.Dexamethasone could suppress NF ?B activation, thus partially blocked the production of cytokines and adhesion molecules,and in turn reduced the damage of inflammatory response. Therefore NF ?B activation might be a key point in the development of smoke inhalation injury and modulation of activation of NF?B might be a potential therapeutic strategy to treat this injury at the transcription level.

To screen genes in endothelial cells resulted from responding to lipopolysaccharide (LPS), mRNA was extracted from both untreated human umbilical endothelial cells (HUVEC) following and HUVEC which were treated with LPS for 6 hours. cDNAs of both populations were synthesized to generate cDNA libraries by suppression subtractive hybridization (SSH). The libraries were then screened with colony dot blots. Positive clones were sequenced and BLAST analysed. The results showed differential genes included 3 novel genes and 22 known genes. The 3 novel genes were confirmed by Northern blotting analysis. These 22 known genes were involved in the regulation of proinflammatory response, cell apoptosis, cytoskeleton, signal transduction and energy metabolism. These results suggest that SSH is an effective technique to detect differential gene expression in HUVEC, which may be helpful to evaluate molecular mechanisms of endothelial injury induced by LPS and provide potential therapeutic targets for LPS related disturbances.