Objective To investigate the protective effects of endotoxin pretreatment on lung injury of rats with endotoxemia. Methods The rat model of acute endotoxemia was established by injecting lipopolysaccharide (LPS) intraperitoneally. Seventy-two male Wistar rats were randomly divided into three groups, ie. a saline control group (N, n=24) , a LPS-treated group (L, n=24) , and a LPS pretreated group ( P, n=24) . Each group was divided into 2 h, 4 h, 6 h, and 12 h subgroups. The rats in group P were firstly administered with introperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were subjected to the injection of 0.5 mg/kg LPS. The rats in group N and L received injection of equivalent amount of saline. After 72 hours, the rats in group L and P were challenged with intravenous injection of 10 mg/kg LPS, otherwise saline in group N. Six rats were killed at 2, 4, 6 and 12 hours respectively after injection of LPS in group L and P. The lungs were removed for detecting intercellular adhesion molecule-1 ( ICAM-1) , superoxide dismutase ( SOD) , and malondialdehyde (MDA) . Meanwhile the level of tumor necrosis factoralpha ( TNF-α) in serum was measured, and the pathological changes of lung were also examined. Results The contents of ICAM-1, MDA and TNF-α in the LPS-treated 4 h group were 75.07 ±0. 53, ( 3.93 ± 0.42) μmol/g, and (478.62 ±45.58) pg/mL respectively, significantly higher than those in the saline control group. The endotoxin pretreatment reduced the above indexes to 42.40 ±0.44, ( 2.89 ±0.49) μmol / g and ( 376.76 ±43.67) pg/mL respectively (Plt;0.05) . The content of SOD in the LPS-treated 4 h group was ( 6.26 ±0.31) U/mg, significantly lower than that in the saline control group. The endotoxin pretreatment increased SOD to ( 8.79 ±0.35) U/mg. Conclusion Endotoxin pretreatment can suppress the progress of lung injury in rats with endotoxemia and protect the lung tissue by down-regulating the inflammatory response and oxygen free radical production.
Objective To observe the histopathologic features and expression patterns of tumor necrosis factor-alpha; （TNF-alpha;）, interleukin-1beta;（IL-1beta;） and Escherichia coli lipopolysaccharide (LPS) in the rat vitreous with LPS inducedendophthalmitis. Methods Wistar rats were randomly divided into saline control group (SC,136 rats）,endophthalmitis group （EO, 168 rats）and blank control group （BC,12 rats）.EO group received an intravitreal injection of 5 mu;l LPS; SC group received 5 mu;l sterile saline and no intervention for BC group.Six,12,24,48, and 72 hours,5 and 7 days after injection, intraocular inflammation were observed and the eyes and vitreous were collected for histopathological examination and measurement of TNF-alpha;, IL-1beta; and LPS expression. Results Severe inflammatory responses in the eyes were observed in EO group between six and 72 hours after LPS injection，ocular inflammation subsided seven days after LPS injection. In the vitreous, a peak neutrophil count was observed at 24 hours （1224.64plusmn;132.2） cells/eye that rapidly declined at 72 hours （342.25plusmn;47.7） cells/eye. The levels of TNF-alpha; and IL-1beta; in EO group were peaked at 24 hours with （996.18plusmn;89.45） and（5556plusmn;1440）pg/ L, respectively；Persisted at 48 hours and began to decline rapidly thereafter. Seven days after LPS injection, levels of TNF-alpha; and IL-1beta; returned to baseline with （22.16plusmn;5.84）and （73.7plusmn;18.7） pg/L, respectively. LPS concentration in EO group decrease rapidly at 72 hours with （11.03plusmn;3.41） ng and disappear on days 7 with (0.22plusmn;0.08) ng after LPS injection.Conclusions Massive neutrophils infiltration, high levels expression of TNF-alpha; and IL-1beta; and spontaneous elimination of bacterial elements in vitreous cavity were major pathologic characteristics in this experimental model. The expression patterns of TNF-alpha;,IL-1beta; were in accord with LPS clearance process.
PURPOSE:To investigate and changes of the retina and the chorid induced by lipopolysaccharide (LPS)in Lewis rats and to compare the results obtained on tissue wholemounts and sections. METHODS:Immunohistochemistry was carried out both on wholemounts of the retina and the chorid-sclera complex and on ocular sections from normal Lewis rats and those after LPS injection. RESULTS:It was shown on the tissue wholemounts that monocytes were attached to retinal blood vessels and emigrated into the choroid as early as 4hrs after LPS injection. Severe involvement of the retina and macrophages into whole area of these tissues.Furthermore increasing number of major histocompatibility complex classⅡ(MHC classⅡ)positive cells was observed in the choroid.The results on tissue sections revealed that the retina and the choroid were both involved as videnced by infiltration of these cells at some time points after LPS injection. CONCLUSION:Wholemount technique provides undoubtful evidences to show that the retina and choroid are primarily and severely involuted after LPS injection.The endotoxin induced uveitis is,for the first time,presumed to be model for human generalized uveitis. （Chin J Ocul Fundus Dis,1996,12:33-36）
ObjectiveTo explore the therapeutic effect of angiotensin-converting enzyme 2 (ACE2) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in a rat model. MethodsTwenty-four Wistar rats were randomly divided into a control group, an ALI group, and an ACE2 group.The rat ALI model was established by intravenous injection of LPS.Then the rats in the ACE2 group received intraperitoneally injection of recombinant rat ACE2 by 0.1 mg/kg immediately after LPS injection.All rats were sacrificed 2 hours later.Rat arterial blood gas was analyzed and wet/dry (W/D) weight ratio of lung tissue was measured.Concentrations of TNF-α, IL-8 and IL-1βin lung tissue homogenates were measured by ELISA.Pulmonary pathological changes were evaluated by hematoxylin-eosin stain under light microscope. ResultsALI induced by LPS was successfully established in the rats.ACE2 pretreatment markedly impoved PaO2 level of the ALI rats(P < 0.05), and decreased the lung W/D ratio(P < 0.05).The concentration of TNF-α, IL-8 and IL-1βin lung tissue homogenates were also inhibited by ACE2.And the lung histopathological changes and score were attenuated in the ACE2 group. ConclusionACE2 treatment has therapeutic effects on ALI induced by LPS.
In this article, the first time use of continuous veno-venous hemofiltration(CVVH) combined with toxic absorption for the treatment of a crush syndrome patient injured in earthquake is described. Correct therapeutic regimen, close observation and prescription condition are crucial for the success of management. The evidence for the application of this method is also discussed in detail.
【Abstract】Objective To study the changes of insulin-like growth factor-1(IGF-1) in serum of patients with obstructive jaundice.Methods The clinical data of 20 patients with obstructive jaundice were collected and the measurement of serum TNFα,ALT, ALP, endotoxin and IGF-1 were performed. Results The serum IGF-1 in obstructive jaundice was significantly lower than that in gallbladder stone(P＜0.01), while endotoxin, TNF-α, ALT，ALP and TB were higher(P＜0.01). After the biliary duct obstruction was removed, the serum IGF1 in obstructive jaundice was significantly higher than that before operation and serum endotoxin， TNF-α, ALT， ALP and TB were significantly lower than that before operation(P＜0.01). A significant negative correlation was found between serum IGF-1 and serum endotoxin in benign obstructive jaundice(r=-0.761, P＜0.01). ConclusionIn obstructive jaundice, endotoxemia can affect the secretion of IGF-1 from liver. IGF-1 can be used as an index to judge the liver function in obstructive jaundice.
Objective To study the change in serum levels of soluble CD14, tumor necrosis factor-α, E-selectin, interleukin-10 and mean arterial pressure, as well as their relationship to infection during the pathophysiologic process in endotoxemia of rabbits. Methods Sixteen rabbits were randomly divided into two groups: group A, as a control group; group B, endotoxemia group. The model of rabbit with endotoxemia were used. Endotoxin at a dose of 1.5 mg/(kg·h) or 3 mg/(kg·h) was continuously infused through external jugular vein within 2 hours, 1 hour respectively. The change of levels of serum soluble CD14, tumor necrosis factor-α, interleukin-10 and E-selectin were observed at 0 (time before infusion of endotoxin), 30, 60, 120, 180, 240, 300 minutes, while mean arterial pressure was measured by polygraphy system. Results In the group B,there was an increase of content of soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin following 30, 120 minutes respectively,and mean arterial pressure was lower than that of group A at same time points. Conclusion The results suggest that soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin may play an important role during the change of infection and that these changes may be closely related with severe infection.
ObjectiveTo investigate the changes of diamine oxidase(DAO) and endotoxin(ET) during the treatment of systemic inflammatory response syndrome with human growth hormone and the relationship between human growth hormone and intestinal mucosal barrier injury. MethodsOne hundred and fortysix patients with systemic inflammatory response syndrome were randomly divided into operative group and nonoperative group, which were again randomly divided into the study group and control group.Plasma concentration of DAO and ET were determined before the treatment and 1 week after the treatment.ResultsPlasma concentration of DAO and ET in study group decreased after treatment with significant difference (P＜0.05，P＜0.01).ConclusionHuman growth hormone can protect intestinal mucosa barrier.
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection, and is the leading cause of death in intensive care unit patients due to limited therapies currently. As is known to all, endotoxin is important in the pathogenesis of sepsis, whereby infection triggers a systemic inflammatory response, resulting in release of pro- and anti-inflammatory cytokines, which are thought to be responsible for the tissue damage that occurs in sepsis patients. Therefore, removing endotoxins is considered as an effective way to improve the conditions of sepsis patients. Both Toraymaxin (PMX) and adsorptive membrane such as oXiris can remove endotoxins by adsorption, and in this review we will summarize current studies, included in vitro study, animal study, and clinical research to show the benefit from endotoxin removal by oXiris, and also give some suggestions about oXiris clinical practice from experienced experts.