A model of traum a shook was established in rats by comminutedly fracturing of the right femur and bleeding of 15% of the body weight.In the 1st hour after injury,the content of malondialdehyde (MDA) of the heart and the lungs increased,the activity of sv.peroxide dismutase (SOD) in the lungs decreased,and the MDA content and SOD activity in hepatic mitochondria increased synchronously.In the 3rd hour after injury,the MDA content increased not only in the heart,the lungs and hepatic mitochondria but also in the liver and the kidneys,and the SOD activity increased in the heart,the kidneys and the intestinal tract but decreased in hepatic mitochondria.There were further marked elevation of MDA content and progressive inhibition on SOD activity in the 5 vital organs and hepatic mitochondria in the 5th hour after injury.When shock continued to progress,the plasma MDA content increased gradually,the SOD activity of the hemolytic blood decreased,and the activities of plasma acid phosphatase and ?-glucuronidase,the indicators of lysosome destruction,increased markedly.These findings suggest that the oxygen-derived free radicals are responsible for the damages to cells of the vital organs and subcellular organelles during traumatic shock.

Objective　To explore the effect of dexamethasone (Dex) given with the intention of prevention or treatment on endotoxin shock in rabbits and its relationship with tumor necrosis factor (TNF). Methods　Fifty-three health rabbits were divided into 4 groups, including normal control (n=13), endoxin shock group (n=16), preventive Dex group (n=12) and therapeutic Dex group (n=12). Except normal control was given with saline, the other 3 groups were administered with lipopolysaccharide (LPS) infusion, and the preventive Dex group was treated with Dex (5 mg/kg body weight) 30 min before LPS infusion and the therapeutic Dex group 20 min after LPS infusion. Mean arterial blood pressure (MABP), survival rate, TNF level in circulatory blood and other parameters were detected. Results　In preventive and therapeutic Dex groups, MABP was increased and survival rate was reduced compared with the animals from endoxin shock group (P<0.05, P<0.01), and TNF activity in the circulating blood was significantly suppressed (P<0.01). In addition, dexamethasone administration could alleviate the elevation of plasma glucagon, glucose, lactic acid, and β-glucironidase (P<0.05, P<0.01) in shocked animals. It was also found that administration of dexamethasone in vitro prevented the release of TNF by Kupffer cells. Conclusion　These results indicate that the preventive and therapeutic effect of dexamethasone on endotoxin shock, which may relate to its direct inhibition of the release of TNF induced by LPS.

AIM: This study aimed at elucidated the possibility that prevent tissue from secondary injury by regulating polymorphonuclear neutrophil (PMN) apoptosis in vitro . METHODS:Neutrophils, isolated from peripheral blood, were incubated with sodium arsenite (Ars), tumor necrosis factor (TNF-?), interleukin-6 (IL-6), burned serum and traumatic serum, respectively. Apoptosis rate, expression of CD11b, respiratory burst and concentration of Ca 2+ were then measured. RESULTS:The elevation of PMN apoptosis rate was Ars concentration dependent, but activated PMN became insensitive to Ars. IL-6 delayed PMN apoptosis (compared with control at 24 h, P

Objective To investigate the effects of limited resuscitation on hepatic ischernia-reperfusion in-jury in rots with hemorrhagic shock. Method Uncontrolled hemorrhagic shock was induced in 54 rats by transect-ing the middle branch of the splenic artery to produce standardized massive splenic injury. Resuscitation started when the mean arterial pressure (MAP) reached 40 mmHg. The rats were randomly divided (n = 9per group) in-to sham-operated group (SS), or one of five treatment groups in which infusion of Ringer' s solution was continually administrated to maintain MAP at 40 (RS40), 50 (RS50), 60 (RS60), 80 (RS80) or 100 mmHg (RS100) for 45 minutes (T45 point). After the bleeding was controlled, resuscitation was continued with Ringer's solution and whole blood (2:1) to increase the MAP to 100 mmHg for 120 minutes (T165 point), which was followed by obser-vation for 240 minutes (T405 point). All animals were observed for 240 minutes or until death. Blood specimens were collected at TO, T45, T165 and T405 for determination of blood lactate levels. At the end of the experiment,a small amount of hepatic tissue was collected to measure tissue blood perfusion, total antioxidative capacity (TAOC), Na+K+ ATPase activity and malondialdehyde (MDA) levels. Results At T405, the blood lactate lev-els in the RS80 and RS100 groups [(3.60±0.68) and (3.84 ± 1.09) mmol/L, respectively] were significantly higher than those in the SS, RS40, RS50 and RS60 groups [(2.00±0.66),(2.74±1.45),(2.43 +0.94) and (2.07±0.95) mmol/L, respectively;all:P < 0.05]. The MDA levels were significantly higher in the RS80 and RS100[(7.32±0.31) and (7.71±0.23) nmol/mg,respectively] than those in the SS, RS40, RS50 and RS60 groups[(4.95±0.80),(6.14±0.94),(6.42±0.48) and (6.84±0.36) nmol/mg, respeetively;all: P <0.05]. The Na+ K+ ATPase and TAOC levels were significantly lower in all of the RS groups than those in the SS group (all: P < 0.05), and those in the RS80 and RS100 groups was significantly lower than those in the RS40,RS50 and RS60 groups (all: P <0.05). Blood perfusion in the RS80 and RS100 groups was significantly lower than that in the other groups (all: P < 0.05). Conclusions If hemorrhage is uncontrolled, limited resuscitation appears to balance the needs for organ perfusion, improve the microcircttlation and decrease lactate levels. Fur-thermore, limited resuscitation could decrease ischemia-reperfusion injury in liver tissue.

Objective　The effects of nitric oxide(NO) on the endotoxin-induced tissue damage,especially intestinal injury and bacterial translocation are still poorly known, although its involvement in vasodilatation and hypotenion in shock is much clear. So, the intestinal damage and bacterial translocation were observed in this study in endotoxemic rats after treatment with Nω-nitro-L-arginine(LNNA),the special inhibitor of NO synthase(NOS),and L-arginine,the substrate of NOS.Methods　The endotoxemia was conducted with administration of lipopolysaccharide(O111B4,10mg/kg,i.p.),animals were treated with LNNA(4mg/kg,i.p.)or L-arg(40mg/kg,i.p.).Intestinal molondialdehyde(MDA) content and Diamine oxidase(DAO) activity were determined,and mesenteric lymph nodes were cultured.Results　The results showed that endotoxin decreased intestinal DAO acitivity but increased MDA content and incidence of bacterial translocation to mesenteric lymph nodes.These effects of endotoxin were aggregated by inhibition of NO production with LNNA, but attenuated by L-arg.Conclusion　We concluded that inhibition of NO formation might enhance endotoxin-induced intestinal damage and bacterial translocation,which suggested that NO might play a protective role in this endotoxemia model.

Objective To study the bio-safety of a multifunctional dressing based on isobutyl-chitosan,a derivative of chitosan.Methods To investigate the local irritation of the multifunctional dressing by skin,subcutaneous and eye application,determine its sensitization by patch test and observe its systemic acute toxicity by abdominal injection.Results The isobutyl-chitosan multifunctional dressing had no irritation,sensitization and systemic acute toxicity.Conclusion The isobutyl-chitosan multifunctional dressing has a good bio-safety as a wound dressing.

OBJECTIVE: To investigate the effect of bactericidal/permeability-increasing protein(BPI) on the outcome of sepsis in mice and its possible mechanism. METHODS: Sepsis was induced by injection of 2x10(6) colony-formed unit E. coli J5 via the tail vein. BPI of 5 mg/kg or equal volume of normal saline(NS) were injected intravenously at the same time. Endotoxin and TNFalpha levels in serum were assayed using a chromogenic limulus amebocyte lysate test and ELISA respectively. RESULTS: Seventy-two hour survival rate of septic mice was significantly higher in the BPI group (15/18) than in the NS group(8/18, P<0.01). Serum endotoxin levels in the BPI group (1.3+/-0.3 and 0.7+/-0.4 &mgr;g/L) were significantly lower than those in the NS group (3.9+/-0.8 and 2.5+/-0.9 &mgr; g/L, P<0.01) 0.5 and 1 hour following injection of bacteria respectively. The peak levels of serum tumor necrosis factor-alpha(TNFalpha)in the BPI group (1.9+/-0.6 &mgr;g/L) were also markedly lower than those in the NS group (3.8+/-0.8 &mgr;g/L, P<0.01) 1.5 hours following bacterial injection. But there was no significant difference in blood bacterial count between the BPI and NS groups 0.5, 1.5 and 3.0 hours after injection of bacteria. CONCLUSIONS: BPI has a marked protective effect on E. coli sepsis, which might be related to its action against bacterial endotoxin and its inhibition of TNFalpha production in sepsis.