Blood gases and pathological changes of lung tissues from patients dying of respiratory failure were observed. The results demonstrated that hypoxemia, hypocapnia, enlarging of A-DO2 and metabolic acidosis occurred soon after severe burns. The severity of falling of PaO2 was positively accorded with burn size (TBSA) . In patients complicated with moderate and severe inhalation injury, severe shock and systemic infections, the reduction of PaO2 was much more pronounced than in those without the above mentioned complications. The failed lung tissues showed congestion, hemorrhage, edema and thrombosis. These findings suggested that besides the severity of burns itself, inhalation injury, severe shock and systemic infections were the main etiological factors invoking postburn lung damage, and the inhalation injury ranked the first. Of the 57 patients 16 developed respiratory failure.The postburn respiratory failure could be classified into three patterns: 1 ).Early pattern, 6 cases (37.5%) , occurring during shock stage. Severe inhalation injury was the main cause) 2). Delayed pattern, 8 cases (50.0%) , developing during acute infection stage of the burn course. Clinical course of this pattern simulated to that of ARDS and the main etiological factors included severe shock and early systemic infections; and 3) .Late pattern, 2 cases (12.5%), occurring during wound healing and rehabilitation ages. The reasons chiefly included severe hypoproteinemia, malnutrition, infect and pulmonary embolism due to thrombosis of inferior vena cera or feora vein.

Smoke inhalation injury was inflicted to 13 goats with chrnoic lung lymph fistula. The contents of thromboxane A2(TXA2) and prostacyclin(PGI2) in plasma, lung lymph fluid, and lung tissues were measured in the 6-hour-periodafter injury with radioimmunoassay. Extravascular lung water(EVLW), thequantity of lymph fluid (QL), the ratio of protein contents in lung lymph and plasma(L/P), hemodynamic parameters, blood gases, platelet count and WBCcount were also determined.It was found that EVLW. QL and L/P increased markedly in the 1st hour, reached the peak of elevation in the 2nd hour, and remained higher than the pre-injury level in the 6th hour after injury, which implies the existence of permea-bility pulmonary edema . Both TXA2 and PGI2 also increased markedly after, injury. The changes of TXA2 and TXA2/PGI2 ratio were in parallelto those of EVLW, QL and L/P in time course and in degree, which implies that the changes of TXA2 and PGI2 might play an important role in the genesis of permeability pulmonary edema. The mechanism might be the direct injury of the two substances and/or the precipitation of platelet and WBC aggregation which can release certain chemical mediators to increase the permeability of the capillaries. In addition, TXA2 might also result in the early elevation of pulmonary arterial pressure.

Mechanical stresses modulate almost all aspects of cell function, including growth, differentiation, migration, gene expression, protein synthesis and apoptosis. Thus, uncovering the mechanisms by which living cells sense and transduce mechanical stress lies at the core of understanding how they respond and adapt to their physical environments. In this review, the possible mechanism about cell response to mechanical stimulus was discussed from outer cell membrane to inner nucleus.

Objective To investigate the relationship between microtubule damage and mitochondria damage in hypoxic cardiomyocytes.Methods Cardiomyocytes from neonatal Wistar rat were isolated and cultured for 3-5 d,then divided into three groups: normal control,hypoxia(cultured in hermetic container containing 1%O_(2),5%CO_(2),95%N_(2)),hypoxia with microtubule depolymerization(by adding 4 ?mol/L colchicine).The fluorescence intensity of ?-microtubule was determined by flow cytometry,the morph and distribution of ?-microtubule and mitochondria were checked by confocal laser scanning microscopy(CLSM) at 30 min,1 h after the cadiomyocytes being oxygen deficit.Results As compared with the normal control cells,the fluorescence intensity of ?-microtubule decreased and the microtubule ruptured and distributed confusedly,and the mitochondria changed into disorder in hypoxic cells.As compared with the hypoxic cells,the distribution of mitochondria confused and the fluorescence intensity decreased in the cells of hypoxia with microtubule depolymerization.Conclusion Microtubule damage occurred at the early stage of hypoxia(30 min).Microtubule damage may lead to mitochondria damage in hypoxic cardiomyocytes.

Objective To explore the effect of c fos antisense gene transfection on the protection of cardiomyocytes following hypoxia and burn serum treatment. Methods Burn serum was collected from Wistar rats with 30% total body surface area(TBSA) of Ⅲ degree burns. The mixture gas containing 1% O 2 was used as hypoxia model. The c fos antisense gene recombinant was constructed by genetic recombination technique. Cardiomyocytes from neonatal Wistar rats were cultured in vitro with hypoxia and burn serum treatment. c fos antisense gene recombinant was transfected into the cultured cardiomyocytes. Expression of c fos mRNA was determined by RT PCR. Expressions of c fos protein, troponin T and ? Tubulin in cardiomyocytes were determined by Western blotting in the transfected and non transfected groups. Results RT PCR results showed that the expression of c fos mRNA increased significantly in the non transfected group. But after transfection of c fos antisense gene recombinant, the expression of c fos mRNA decreased significantly as compared with the non transfected cardiomyocytes. Western blotting results showed that the expression of c fos protein in the transfected group decreased remarkably as compared with the non transfected group, but the expressions of ? Tubulin and troponin T increased significantly in the transfected group. Conclusion Burn serum and hypoxia can cause the injury of cardiomyocytes. c fos antisense gene recombinant transfection has the protective effect on cardiomyocytes exposed to burn serum and hypoxia.

Objective To explore the relation of c jun antisense gene transfection and cardiomyocyte apoptosis following hypoxia and burn serum treatment Methods Burn serum was collected from Wistar rats with 30% total body surface area(TBSA) Ⅲ degree burn Rats inhaling mixed gas containing 1% O 2 was used as hypoxia model The c jun antisense gene recombinant was constructed by genetic recombination technique Cardiomyocytes from neonatal Wistar rats were cultured in vitro with hypoxia and burn serum treatment c jun antisense gene recombinant was transfected into the cultured cardiomyocytes Cardiomyocytes were stained with TUNEL for the examination of cardiomyocyte apoptosis at 12, 24 and 48 h after hypoxia and burn serum treatment In addition, the number of apoptotic cardiomyocytes was counted The results were processed statistically Results In the group with only the addition of burn serum and hypoxia(non transfected group), the numbers of apoptotic cardiomyocytes(mean per high power visual field) were 7 1?0 842, 28 4?1 635 and 13 2?1 525, respectively But after transfection of c jun antisense gene recombinant, numbers of apoptotic cardiomyocytes were 4 1?0 716,12 3?1 455 and 8 5?1 341, respectively There was a significant difference between the transfected group and the non transfected group( P

Objective To explore the molecular mechanism of c-jun antisense gene transfection in protecting cardiomyocytes from injury of hypoxia and burn serum treatment. Methods Burn sera were collected from wistar rat with 30% total body surface area(TBSA) Ⅲ degree burn injury, and the mixture gas containning 1% O 2 was used as hypoxia model. The c-jun antisense gene recombinant vector was constructed. Neonatal wistar rat cardiomyocytes cultured in vitro were treated with hypoxia and burn sera. c-jun antisense gene recombinant vector was transfected into the cultured cardiomyocytes. Expressions of c-jun, PKC? and JNK were detected with western blot in the transfected and non-transfected cardiomyocytes. Results Expression levels of c-jun, PKC? and JNK significantly increased in the non-transfected cardiomyocytes when treated by hypoxia and burn sera, up to maximum 24 hour after the treatment. Expression levels of c-jun, PKC? and JNK in the transfected cardiomyocytes decreased significantly compared with non-transfected cells. Conclusions The transfection of the c-jun antisense gene recombinant vector protected cardiomyocytes from injury of hypoxia and burn sera treatment via down-regulating PKC? and JNK expressions.

Objective To study the effects of ulinastatin (UTI) on the inflammatory cytokines in the blood serum of rats after severe burn. Methods A total of 96 SD rats, inflicted with 30% TBSA full thickness skin burn, were randomly divided into simple burn group (group B) and UTI treated group (group UTI). The serum contents of IL 1?, IL 6, and TNF ? were determined at 0, 1, 3, 6, 12, and 24 h before and after burn injury. Results In group B, the levels of serum IL 1?, IL 6, and TNF ? were significantly higher at 3 h and peaked at 6 and 12 h after burn. In group UTI, the levels of serum IL 1?, IL 6, and TNF ? were significantly lower than those in group B ( 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

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