Protective effect of albumin on lung injury in traumatic/ hemorrhagic shock rats

Objective. To determine the effect of albumin administration on lung injury in traumatic/hemorrhagic shock （T/HS） rats. Methods： Forty-eight adult Sprague-Dawley rats were divided into three groups randomly （ n = 16 in each group） ： Group A, Group B, Group C. In Group A, rats underwent laparotomy without shock. In Group B, rats undergoing T/HS were resuscitated with their blood plus lactated Ringer＇s （twice the volume of shed blood ）. In Group C, rats undergoing T/HS were resuscitated with their shed blood plus additional 3 ml of 5% human albumin. The expression of polymorphonuclear neutrophils CD18/CD11b in jugular vein blood was evaluated. The main lung injury indexes （the activity of myeloperoxidase and lung injury score） were measured. Results： Significant differences of the expression of CD18/11b and the severity degree of lung injury were found between the three groups. （P〈0.05）. The expression of CD18/CD11b and the main lung injury indexes in Group B and Goup C incresed significantly compared with those in Group A （P 〈0.05）. At the same time, the expression of CD18/CD11b and the main lung injury indexes in Group C decreased dramatically, compared with those in Group B （ P 〈0.05 ）. Conclusions ： The infusion of albumin during resuscitation period can protect lungs from injury and decrease the expression of CD18/CD11b in T/HS rats.     

Detection of gene expression pattern in the earyly stage after spinal cord injury by gene chip

Objective:To study the changes of the gene expression pattern of spinal cord tissues in the early stage after injury by DNA microarray (gene chip).Methods:The contusion model of rat spinal cord was established according to Allen‘s falling strike method and the gene expression patterns of normal and injured spinal cord tissues were studied by gene chip.Results:The expression of 45 genes was significantly changed in the early stage after spinal cord injury, in which 22 genes up-regulated and 23 genes down-regulated.Conclusions:The expression of some genes changes significantly in the early stage after spinal cord injury, which indicates the complexity of secondary spinal cord injury.     

七氟烷后处理对大鼠肺缺血再灌注损伤的影响

Objective To investigate the effects of aevoflurane postconditioning on lung iscbemia-reperfusion (IR) injury in rats and the mechanism involved. Methods Ninety-six male SD rots weighing 270-330 g were randomly divided into 4 groups (n = 24 each): sham operation group (group S), group IR, sevoflurane preconditioning group (group SPr), and sevoflurane postconditioning group (group SPo). The animals were anesthetized with intraperitoneal 10% chloral hydrate 400 mg/kg, tracheostomized and mechanically ventilated. Lung IR was produced by occlusion of the hilum of the left lung for 45 min and then it was unclamped for reperfusion, in group SPr, sevoflurane was inhaled at the end-tidal concentration of 2.1% 30 min before lung ischemia. In group SPo, sevoflurane was inhaled at the end-tidal concentration of 2.1% immediately before reperfusiun. Six rats from each group were sacrificed at 30 min, 1 h, 2 h, and 4 h of reperfnsion respectively. The TNF-α, IL-1 and IL-6 concentrations, and WBC count in broncho-alveolar lavage fluid (BALF) were determined.The percentage of PMN in WBC was calculated. The lungs were removed for determination of the cdntent of TNF-α, IL-1 and IL-6 in the lung tissues and microscopic examination. The apoptosis index (AI) was calculated by TUNEL assay. Lung injury was scored. Results The levels of TNF-α, IL-1 and IL-6 in lung tissues and BALF, AI, WBC count, percentage of PMN, and lung injury scores were significantly higher in group IR than in group S (P < 0.01). The content of TNF-α, IL-1 and IL-6 in lung tissues was significantly higher in group SPr and SPo than in group S (P < 0.01). The indices mentioned above were all significantly lower in group SPr and SPo than in group IR (P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group SPr and SPo (P > 0.05). Conclusion Sevoflurane postconditioning can protect the lungs from IR injury by decreasing the inflammatory reaction and inhibiting the apoptosis in pulmonary vascular endothelial and alveolar epithelial cells, and the effect is similar to that of sevoflurane preconditioning.     

mRNA and protein expression of transcription factor c—fos in burned rats and their effects on wound healing

Objective:To explore the expression of mRNA and its protein in burned rats and their effects of burn wound healing.Methods:A partial-thickness burn of 30% total body surface area was created on the back of 40 Wistar rats.In situ hybridization and immunohistochemical methods were used to exaluate the location and the amount of the c-fos mRNA and its protein in normal skin and the burned skin,respectively,at 3h,6h,1d,3d,7d and 14d after burn.Results:Under a light microscope,both the expression of c-for mRNA and its protein could be found in the normal skin,but their induction levels were much higher in the burned skin.The level of for protein expression reached peak at 3h after burn while that of c-for mRNA reached peak at 6h after burn.Conclusions:The expression of c-fos can be induced by burns.And the peak level expression of c-for mRNA comes later than that of c-fos protein.It indicates that the action of fos protein is induced by post-translational modification of pre-existing fos molecules.     

Effect of substance P released from peripheral nerve ending on endogenous expression of epidermal growth factor and its receptor in wound healing

Objective: To explore the relationship between substance P (SP) released from peripheral nerve endings and the expression of epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) during wound bealing. Methods: Fifty Wistar rats were randomly divided into 2 groups, injury group and capsaicin group. In the injury group, a full-thickness skin wound on the back of the rat was taken. The wound edge and granulation tissues were taken on the 1st, 3rd, 6th, 9th, 12th days after injury, respectively. In the capsaicin group, capsaicin was injected subcutaneously on the back of the rats to destroy the sensory nerve to prevent the secretion of SP, then a wound and sample was made in the same way.Immunohistochemistry and in situ hybridization were employed to detect the expression of SP, EGF/EGFR, and EGF mRNA/EGFR mRNA in the granulation tissues.Results: In the injury group,immunohistochemical stain of SP and EGF/EGFR was located on the hair follicles and sebaceous glands at the 1st day. And the stain of SP was obvious at the 3rd day in the granulation tissues, then decreased gradually. EGF/EGFR was at low level at the 3rd day, then increased gradually and reached the peak at the 9th day, then declined. In the capsaicin group, the stain of SP and EGF/EGFR was faint and without obvious change during the wound healing process. The tendency of the EGF mRNA/EGFR mRNA expression was similar to that of EGF/EGFR. Conclusions: During wound healing, SP may promote the healing process by affecting the expression of EGF/EGFR in the erunuation tissues.     

虫草多糖预先给药对大鼠内毒素性急性肺损伤的影响

Objective To evaluate the effects of Cordyceps polysaccharide (CP) pretreatment on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male SD rats were randomly divided into 5 groups ( n = 8 each) : CP1-3 group, ALI group and control group (group C). Group CP1-3 received CP 1, 2 and 3 g/kg by intragastric gavage every 12 h for 6 times respectively, and then received LPS 5 mg/kg iv through the femoral vein 2 h after the last administration. Croup ALI received normal saline 1 ml/100 g instead of CP, and the rest methods were the same as those described in group CP. Group C received normal saline 1 ml/100 g instead of CP and LPS, and the rest methods were the same as those described in group CP. The animals were killed 6 h after injection of LPS. The lungs were removed for determination of W/D lung weight ratio, pulmonary permeability index (PPI), WBC and PMN counts in broncho-alveolar lavage fluid (BALF) , and levels of TNF-α in lung tissues and BALF, and microscopic examination.Results Compared with group C, W/D lung weight ratio, PPI, WBC and PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly increased in group ALI and CP1-3 ( P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group CP1 and group ALI ( P > 0.05) . The indices mentioned above were significantly lower in group CP2,3 than in group ALI ( P < 0.05) . PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly lower in group CP3 than in group CP2 ( P < 0.05) . Conclusion Cordyceps polysaccharide pretreatment can attenuate LPS-induced ALI in a dose-dependent manner through inhibition of inflammatory response in rats.     

虫草多糖预先给药对大鼠内毒素性急性肺损伤的影响

Objective To evaluate the effects of Cordyceps polysaccharide (CP) pretreatment on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male SD rats were randomly divided into 5 groups ( n = 8 each) : CP1-3 group, ALI group and control group (group C). Group CP1-3 received CP 1, 2 and 3 g/kg by intragastric gavage every 12 h for 6 times respectively, and then received LPS 5 mg/kg iv through the femoral vein 2 h after the last administration. Croup ALI received normal saline 1 ml/100 g instead of CP, and the rest methods were the same as those described in group CP. Group C received normal saline 1 ml/100 g instead of CP and LPS, and the rest methods were the same as those described in group CP. The animals were killed 6 h after injection of LPS. The lungs were removed for determination of W/D lung weight ratio, pulmonary permeability index (PPI), WBC and PMN counts in broncho-alveolar lavage fluid (BALF) , and levels of TNF-α in lung tissues and BALF, and microscopic examination.Results Compared with group C, W/D lung weight ratio, PPI, WBC and PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly increased in group ALI and CP1-3 ( P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group CP1 and group ALI ( P > 0.05) . The indices mentioned above were significantly lower in group CP2,3 than in group ALI ( P < 0.05) . PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly lower in group CP3 than in group CP2 ( P < 0.05) . Conclusion Cordyceps polysaccharide pretreatment can attenuate LPS-induced ALI in a dose-dependent manner through inhibition of inflammatory response in rats.     

虫草多糖预先给药对大鼠内毒素性急性肺损伤的影响

Objective To evaluate the effects of Cordyceps polysaccharide (CP) pretreatment on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male SD rats were randomly divided into 5 groups ( n = 8 each) : CP1-3 group, ALI group and control group (group C). Group CP1-3 received CP 1, 2 and 3 g/kg by intragastric gavage every 12 h for 6 times respectively, and then received LPS 5 mg/kg iv through the femoral vein 2 h after the last administration. Croup ALI received normal saline 1 ml/100 g instead of CP, and the rest methods were the same as those described in group CP. Group C received normal saline 1 ml/100 g instead of CP and LPS, and the rest methods were the same as those described in group CP. The animals were killed 6 h after injection of LPS. The lungs were removed for determination of W/D lung weight ratio, pulmonary permeability index (PPI), WBC and PMN counts in broncho-alveolar lavage fluid (BALF) , and levels of TNF-α in lung tissues and BALF, and microscopic examination.Results Compared with group C, W/D lung weight ratio, PPI, WBC and PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly increased in group ALI and CP1-3 ( P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group CP1 and group ALI ( P > 0.05) . The indices mentioned above were significantly lower in group CP2,3 than in group ALI ( P < 0.05) . PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly lower in group CP3 than in group CP2 ( P < 0.05) . Conclusion Cordyceps polysaccharide pretreatment can attenuate LPS-induced ALI in a dose-dependent manner through inhibition of inflammatory response in rats.     

虫草多糖预先给药对大鼠内毒素性急性肺损伤的影响

Objective To evaluate the effects of Cordyceps polysaccharide (CP) pretreatment on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male SD rats were randomly divided into 5 groups ( n = 8 each) : CP1-3 group, ALI group and control group (group C). Group CP1-3 received CP 1, 2 and 3 g/kg by intragastric gavage every 12 h for 6 times respectively, and then received LPS 5 mg/kg iv through the femoral vein 2 h after the last administration. Croup ALI received normal saline 1 ml/100 g instead of CP, and the rest methods were the same as those described in group CP. Group C received normal saline 1 ml/100 g instead of CP and LPS, and the rest methods were the same as those described in group CP. The animals were killed 6 h after injection of LPS. The lungs were removed for determination of W/D lung weight ratio, pulmonary permeability index (PPI), WBC and PMN counts in broncho-alveolar lavage fluid (BALF) , and levels of TNF-α in lung tissues and BALF, and microscopic examination.Results Compared with group C, W/D lung weight ratio, PPI, WBC and PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly increased in group ALI and CP1-3 ( P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group CP1 and group ALI ( P > 0.05) . The indices mentioned above were significantly lower in group CP2,3 than in group ALI ( P < 0.05) . PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly lower in group CP3 than in group CP2 ( P < 0.05) . Conclusion Cordyceps polysaccharide pretreatment can attenuate LPS-induced ALI in a dose-dependent manner through inhibition of inflammatory response in rats.     

虫草多糖预先给药对大鼠内毒素性急性肺损伤的影响

Objective To evaluate the effects of Cordyceps polysaccharide (CP) pretreatment on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty adult male SD rats were randomly divided into 5 groups ( n = 8 each) : CP1-3 group, ALI group and control group (group C). Group CP1-3 received CP 1, 2 and 3 g/kg by intragastric gavage every 12 h for 6 times respectively, and then received LPS 5 mg/kg iv through the femoral vein 2 h after the last administration. Croup ALI received normal saline 1 ml/100 g instead of CP, and the rest methods were the same as those described in group CP. Group C received normal saline 1 ml/100 g instead of CP and LPS, and the rest methods were the same as those described in group CP. The animals were killed 6 h after injection of LPS. The lungs were removed for determination of W/D lung weight ratio, pulmonary permeability index (PPI), WBC and PMN counts in broncho-alveolar lavage fluid (BALF) , and levels of TNF-α in lung tissues and BALF, and microscopic examination.Results Compared with group C, W/D lung weight ratio, PPI, WBC and PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly increased in group ALI and CP1-3 ( P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group CP1 and group ALI ( P > 0.05) . The indices mentioned above were significantly lower in group CP2,3 than in group ALI ( P < 0.05) . PMN counts in BALF, lung pathological scores and levels of TNF-α in lung tissues and BALF were significantly lower in group CP3 than in group CP2 ( P < 0.05) . Conclusion Cordyceps polysaccharide pretreatment can attenuate LPS-induced ALI in a dose-dependent manner through inhibition of inflammatory response in rats.     

烧伤后粘附分子介导中性粒细胞粘附对肺血管通透性的影响

目的观察比较烧伤血清及烧伤后中性白细胞（ＰＭＮ）对肺血管通透性的影响,分析ＰＭＮ粘附及粘附分子ＣＤ１１ｂ／ＣＤ１８在该影响中的介导作用。方法应用离体肺灌流技术,通过肺重量增加（ＬＷＧ）、液体滤过系数（Ｋｆ）和通透性表面积乘积（ＰＳ）分别观察肺水肿程度、肺血管对小分子物质和大分子物质的通透性。结果烧伤血清能使ＬＷＧ、Ｋｆ和ＰＳ明显增加,以Ｋｆ增加最为明显;烧伤后ＰＭＮ也能使Ｋｆ和ＰＳ增加,以ＰＳ增加为明显;用单抗封闭烧伤后ＰＭＮ膜上ＣＤ１１ｂ／ＣＤ１８后,ＰＭＮ在肺血管内的滞留减少,Ｋｆ和ＰＳ值增加被抑制,并以ＰＳ改变为显著。结论（１）被激活的ＰＭＮ释放的介质类物质如氧自由基、蛋白酶等物质对肺微血管内皮细胞（ＰＭＥＣ）的损伤作用部分依赖于ＰＭＮ与内皮细胞的粘附。（２）烧伤后被激活的ＰＭＮ释放的介质类物质主要介导肺血管对小分子物质通透性的影响。烧伤后ＰＭＮ与肺微血管内皮细胞（ＰＭＥＣ）的粘附除了使介质类物质的作用放大外,还介导肺血管对大分子物质通透作用。（３）ＰＭＮ膜上ＣＤ１１ｂ／ＣＤ１８分子可能通过与ＰＭＥＣ细胞间粘附分子的结合,本身具有对内皮细胞的生物学调控作用     

CD11／CD18在烧伤早期中性粒细胞对内皮细胞粘附中的…

为了解烧伤早期病人中性粒细胞（ＰＭＮ）膜表面ＣＤ１１ａ／ＣＤ１８和ＣＤ１１ｂ／Ｃｄ１８变化规律及其在烧伤早期ＰＭＮ对内皮细胞（ＥＣ）粘附及损伤中的作用，为临床抗白细胞粘附治疗提供依据，将烧伤早期ＰＭＮ与体外培养的人脐静脉内皮细胞（ＨＵＶＥＣ）孵育２４小时后，观察烧伤早期ＰＭＮ与ＥＣ粘附百分率和烧伤早期ＰＭＮ引起内皮细胞单层流出液生成速率（Ｊｖ）和滤过系数（ｋｆ）变化，ＣＤ１１／ＣＤ１８单抗（ｍＡｂ     

Dynamics of leukocyte receptors after severe burns: an exploratory study

Background

Patients with burns are susceptible to organ failure, and there is indirect evidence that leukocytes may contribute to this process. They may change the expression of cell-surface receptors after certain stimuli, for example, the burn. We therefore aimed to assess the changes induced by the burn in the expression of leukocyte cell-surface receptors CD11b, CD14, CD16, and CD62L on the surface of PMNs and monocytes. We also wanted to examine the dynamics of this activation during the first week after the burn, and to relate it to the size of the injury.

Methods

Ten patients with burns of >15% (TBSA) were included in the study. Blood samples were collected on arrival and every consecutive morning during the first week. Healthy volunteers acted as controls.

Results

PMN CD11b expression was increased. The extent of PMN CD11b expression correlated negatively to the size of the full thickness burn. Monocyte CD14 expression increased initially but there was no relation to the size of the burn. PMN CD16 expression decreased initially during the first days and the decrease was related to burn size. CD62L did not vary depending on the burn in either PMN or monocytes during the first week after the burn.

Conclusion

This study showed that specific receptors on the surface of leukocytes (PMN CD11b, monocyte CD14 and PMN CD16) are affected by the burn. Expression of PMN CD11b and CD16 are related to burn size. Burn-induced effects on the expression of PMN receptors, such as PMN CD11b and CD16, may contribute to burn-induced infection susceptibility.     

Dietary restriction impairs neutrophil exudation by reducing CD11b/CD18 expression and chemokine production

HYPOTHESIS: Patients with malnutrition are susceptible to infection. Polymorphonuclear neutrophils (PMNs) are the major effector of the nonspecific immune response in host resistance to infection. Dietary restriction may impair PMN-mediated immunity in the peritoneal cavity by reducing PMN exudation, adhesion molecule expression on PMNs, and chemokine production. DESIGN: Randomized study of murine glycogen-induced peritonitis with dietary restriction. SETTING: University research laboratory. MATERIALS: Male C57BL/6J mice. INTERVENTIONS: Mice (N = 204) were assigned to ad libitum, moderate, and severe diet-restricted groups receiving mouse chow ad libitum (132 g/kg, 66 g/kg, and 33 g/kg daily for 7 days, respectively). After dietary restriction with or without 1 day of refeeding, mice were administered glycogen intraperitoneally to induce cell exudation. MAIN OUTCOME MEASURES: CD11b, CD18, and CD62L expressions on circulating PMNs, phagocytosis, and reactive oxygen intermediate production by exudative PMNs were measured after glycogen installation. The levels of PMN-specific chemokine, macrophage inflammatory protein 2 (MIP-2), in peritoneal lavage fluid were also measured. These parameters were measured after glycogen installation in the refeeding experiment. RESULTS: Seven days of dietary restriction decreased CD11b/CD18 expression on circulating PMNs, MIP-2 levels in peritoneal lavage fluid, and subsequent PMN exudation into the peritoneal cavity early in peritonitis. Both CD11b and CD18 expression on circulating PMNs and MIP-2 levels correlated significantly with numbers of exudative PMNs. Seven days of dietary restriction also impaired phagocytosis, while up-regulating reactive oxygen intermediate production by exudative PMNs. Only 1 day of ad libitum refeeding normalized CD11b/CD18 expression with PMN exudation into the peritoneal cavity. CONCLUSIONS: Short-term dietary restriction impairs PMN exudation into local inflammatory sites in murine peritonitis by reducing CD11b/CD18 expression and MIP-2 production. Even brief nutritional replenishment in diet-restricted patients may improve host defense via restoring these PMN functions and chemokine production at local inflammatory sites.     

内毒素性肺损伤外周血中性粒细胞CD11b表达的意义

目的：探讨内毒素血症大鼠外周血中性粒细胞（PMN）表面CD11b表达与内毒素性肺损伤的关系。方法：大肠杆菌E-Coli O111B4 4mg／kg尾静脉注射制备大鼠内毒素血症动物模型。112只大鼠随机分为对照组（静脉注射等量生理盐水）及内毒素注射后1h组、2h组、4h组、8h组、12h组、24h组,每组16只动物。在相应时间点放血处死动物,分别取股静脉血、肺组织及进行支气管肺泡灌洗,测定肺组织湿／干重（W／D）比值、肺组织髓过氧化物酶（MPO）活性和支气管肺泡灌洗液（BALF）总蛋白定量等肺损伤指标。流式细胞仪测定外周血PMN表面CD11b表达。另取16只大鼠,内毒素注射后2h时测定外周血PMN表面CD11b表达,24h时放血处死,测定上述指标。结果：①大鼠内毒素血症可以造成明显的急性肺损伤,表现为肺组织W／D比值、MPO活性和BALF总蛋白明显增高,分别在2h、8h和2h显著高于对照组（P〈0．05或P〈0．01）,峰值分别出现在内毒素注射后12h、24h和12h;②大鼠内毒素性肺损伤时,外周血PMN表面CD11b表达水平在早期（1h）明显升高（与对照组比较,P〈O．05）,在2h达到峰值,之后逐渐降低;③外周血CD11b表达峰值明显早于肺组织W／D比、MPO和BALF总蛋白等肺损伤指标的峰值出现时间;④同一动物2h时外周血PMN表面CD11b的表达水平与其24h时肺组织W／D比、MPO和BALF总蛋白含量呈显著正相关（r分别为0．78、0．77和0．73,P〈0．05）。结论：内毒素性肺损伤中,外周血CD11b表达升高可能有助于内毒素性肺损伤的早期诊断,并可能预示以后的肺损伤程度。     

烧伤后白细胞与内皮细胞粘附分子介导作用的研究

为研究白细胞粘附依赖于细胞粘附分子的介导作用,作者通过离体实验观察分析了烧伤血清对外周血中性粒细胞（ＰＭＮ）ＣＤ１１ｂ／ＣＤ１８表达的影响及ＣＤ１１ｂ／ＣＤ１８在烧伤后ＰＭＮ粘附中的介导作用。结果表明：（１）烧伤血清使ＰＭＮＣＤ１１ｂ／ＣＤ１８分子表达和ＰＭＮ与肺微血管内皮细胞（ＰＭＥＣ）的粘附率增高。（２）ＣＤ１１ｂ／ＣＤ１８单抗不仅能使正常ＰＭＮ与ＰＭＥＣ的粘附率下降５０％,也使烧伤血清激活的ＰＭＮ与ＰＭＥＣ粘附率下降至烧伤血清激活前水平。我们认为,严重烧伤能使外周血ＰＭＮＣＤ１１ｂ／ＣＤ１８表达明显增高,ＣＤ１１ｂ／ＣＤ１８不但介导基础状态下的ＰＭＮ粘附,更是介导烧伤后引起的大量ＰＭＮ与ＰＭＥＣ粘附的主要分子。     

皮肤撕脱伤中CD11b、ICAM-1动态表达的实验研究

目的：通过对皮肤撕脱伤动物模型中粘附分子CD11b、ICAM－1动态表达的研究，探讨皮肤撕脱伤继发性坏死的机理。方法：在猪后肢碾压形成潜行皮肤撕脱伤动物模型，在撕脱区切取撕脱皮瓣，在对侧肢体切取正常任意皮瓣作为对照。用SP法检测撕脱伤后0、2、6、12、24h外周血中性粒细胞膜表面CD11b及组织中血管内皮细胞膜表达ICAM－1的表达，并进行半定量分析，了解二者的动态变化。结果：撕脱组CD11b及ICAM－1随时间推移逐渐升高，至12h达高峰，24h后有所下降，撕脱组的表达明显高于对照组。结论：撕脱伤中粘附分子CD11b及ICAM－1呈高表达，二者可能参与了随后发生的撕脱皮瓣的继发性坏死。     

Reduced expression of neutrophil CD11b and CD16 after severe traumatic injury.

Overwhelming sepsis continues to be a major source of morbidity and mortality in patients who have sustained severe traumatic injury. Recently, much interest has been focused on the role of the peripheral blood neutrophil (PMN) in infections in these patients. Two surface receptors, CD11b (CR3) and CD16 (Fc gamma RIII), are thought to participate in bacterial phagocytosis and are both present on greater than 85% of normal PMNs. We have previously shown that cells that lack both of these receptors have markedly reduced phagocytic function. The purpose of this study was to determine the effect of severe trauma on the expression of these PMN receptors. Twenty severe trauma patients, age 19-70 years, presenting with an initial APACHE II score of greater than or equal to 10 were arbitrarily divided into two groups to define severity of injury: Group A, initial APACHE II of 10-18 (n = 11) and Group B, initial APACHE II of 19-25 (n = 9). Blood was obtained on admission, on Day 3, and weekly thereafter. PMNs were stained with fluorochrome-labeled monoclonal antibodies directed against CD11b and CD16 and then analyzed by flow cytometry. Controls consisted of 14 normal adults, age 20-65 years. The percentage and absolute numbers of CD11b+/CD16+ PMNs were determined for each patient or control sample. ANOVA and multiple comparison of variables (P = 0.05) were performed for each week. Values for Group A were different from controls at Weeks 0, 1, and 3. Values for Group B were significantly lower than those of controls at all weeks.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lipopolysaccharide-binding protein and lipopolysaccharide receptor CD14 gene expression after thermal injury and its potential mechanism(s)

BACKGROUND: We hypothesized that lipopolysaccharide-binding protein (LBP) and lipopolysaccharide receptor CD14 would present a pair of key molecules in pathophysiologic alterations induced by low concentrations of endotoxin after trauma. The aim of this study was to investigate the relationship between endotoxin translocation and tissue LBP/CD14 messenger ribonucleic acid (mRNA) expression after burn injury, and to define the potential role of LBP/CD14 in mediating inflammatory mediator induction, as well as the pathogenesis of organ damage. METHODS: Wistar rats were subjected to a 35% full-thickness scald injury, and tissue samples from liver, kidneys, lungs, and intestine were collected to measure LBP/CD14 and tumor necrosis factor-alpha (TNF-alpha) mRNA expression. Peritoneal macrophages were harvested by peritoneal lavage to determine CD14 mRNA expression. RESULTS: It was found that endotoxin levels in liver, spleen, and lung increased markedly after thermal injury, with the highest level in liver. Both tissue LBP and CD14 mRNA expression increased markedly after burns, peaking at 12 hours, and then decreasing gradually. At 48 hours, LBP gene expression had a tendency to the baseline level, whereas CD14 mRNA expression increased again. Likewise, CD14 mRNA levels were up-regulated markedly in peritoneal macrophages. Conversely, gene expression of TNF-alpha in tissues elevated markedly after acute insults. There were positive correlations between lipopolysaccharide levels and LBP/CD14 mRNA as well as TNF-alpha mRNA expression in tissues. Similar results were also obtained between CD14, TNF-alpha mRNA expression in liver tissue and liver function parameters, and between pulmonary TNF-alpha mRNA and myeloperoxidase activities (p < 0.01). CONCLUSION: Thermal injury per se can markedly up-regulate both LBP and CD14 gene expression in various organs. Excessive LBP and CD14 mRNA expression might be associated with enhanced synthesis and release of TNF-alpha stimulated by endotoxin translocation after major burns.     

Mesenteric lymph is responsible for post-hemorrhagic shock systemic neutrophil priming.

BACKGROUND: Hemorrhagic shock-induced splanchnic hypoperfusion has been implicated as a priming event in the two event model of multiple organ failure (MOF). We have previously shown that early postinjury neutrophil (PMN) priming identifies the injured patient at risk for MOF. Recent in vitro studies have demonstrated that postshock mesenteric lymph primes isolated human neutrophils. We hypothesize that lymphatic diversion before hemorrhagic shock abrogates systemic PMN priming and subsequent lung injury. METHODS: Sprague-Dawley rats (n >or= 5 per group) underwent hemorrhagic shock (MAP 40 mm Hg x 30 min) and resuscitation (shed blood + 2x crystalloid) with and without mesenteric lymphatic duct diversion. Sham animals underwent anesthesia and laparotomy. Whole blood was taken 2 hours after resuscitation, heparinized, and incubated for 5 min at 37 degrees C. Surface expression of CD11b (a marker for PMN priming) was determined by flow-cytometry compared with isotype controls. In addition, lung myeloperoxidase (MPO) was measured for PMN sequestration, and Evans blue lung leak was assessed in the bronchoalveolar lavage fluid in sham, and shock +/- lymph diversion animals. RESULTS: Hemorrhagic shock resulted in increased surface expression of PMN CD11b relative to sham (23.8 +/- 6.7 vs. 9.9 +/- 0.6). Mesenteric lymphatic diversion before hemorrhagic shock abrogated this effect (8.0 +/- 2.6). Lung PMN accumulation, as assessed by MPO, was greater in the lungs of nondiverted (113 +/- 14 MPO/mg lung) versus sham (55 +/- 4 MPO/mg lung, p < 0.05); lymph diversion reduced lung PMNs to control levels (71 +/- 6.5 MPO/mg lung, p < 0.05). Evans blue lung leak was 1.6 times sham in the hemorrhagic shock group; this was returned to sham levels after lymph diversion (p < 0.05). CONCLUSION: Post-hemorrhagic shock mesenteric lymph primes circulating PMNs, promotes lung PMN accumulation, and provokes acute lung injury. Lymphatic diversion abrogates these pathologic events. These observations further implicate the central role of mesenteric lymph in hemorrhagic shock-induced lung injury. Characterizing the PMN priming agents could provide insight into the pathogenesis of postinjury MOF and ultimately new therapeutic strategies.