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1.
AIM: To investigate the protective effect of anti-macrophage migration factor monoclonal antibody (anti-MIF MAb) on oleic-acid-induced acute lung injury (ALI) rats and its influence on the expression level of MIF and intercellular adhesion molecule-1(ICAM-1). METHODS: The rats were subjected to injection of oleic acid (oleic acid group) or saline solution (control group). One hours before administration of oleic acid, the rats were intraperitoneally injected with anti-MIF antibody (5 mg/kg) as the treatment group. After injecting oleic acid or saline for 4 hours, the PaO2, lung permeability index (LPI), the number of macrophage and the level of soluble ICAM-1 (sICAM-1) in the bronchial alveolar lavage fluid (BALF) were measured. The expression level of MIF mRNA and ICAM-1 mRNA in the lung were detected by in situ hybridization, and the degree of macrophage infiltration and the expression of MIF were evaluated by double staining immunocytochemistry. RESULTS: The PaO2 of the oleic acid group was far lower than those of the control and treatment group (P<0.01). The LPI of the oleic acid group was significantly higher than those of the control and treatment group (P<0.01). The sICAM-1 level in BALF were significantly higher than those of the control and treatment groups (P<0.01). There were marked up-regulation of MIF mRNA and ICAM-1 mRNA expression in ALI lung compared with the normal lung tissue. After pretreatment with anti-MIF antibody, the MIF expression was down-regulation in association with a marked reduction of macrophage infiltration. However, pretreatment with anti-MIF antibody did not interfere the expression level of ICAM-1. CONCLUSION: MIF and ICAM-1 may mediate the infiltration and adhesion of macrophage in injuried lung tissue, which play a pivotal role in the pathogenesis of progressive lung injuries induced by intravenous oleic acid. Pretreatment with anti-MIF antibody showed lung protective effect by blockage of MIF expression in association with reduction of macrophage infiltration and improvement in histological damage.  相似文献   

2.
会讯     
AIM:To investigate the pulmonary expresson of macrophage migration inhibitory factor(MIF) in acute lung injury (ALI) rats induced by intravenous injection of oleic acid and its correlation with blood gas change, pulmonary weight index (PWI) and pulmonary pathological injuries.METHODS: ALI rats model were made by injecting oleic acid as the oleic acid group while rats injection with saline solution as control. After injecting oleic acid or saline for six hours, the PaO2 and PaCO2 of the left heart and pulmonary weight index were measured. At the same time, by using a microwave-base double immunohistochemistry labeling, the number of MIF＋, ED1+ (anti-CD68 antibody), ED1+/MIF＋cell in pulmonary tissue of different groups and their correlation with blood gas and pulmonary weight index were examined. RESULTS: The blood gas parameters of the oleic acid group were far worse than that of the control group (P＜0.01). The PWI of the oleic acid group was significantly higher than that of the control group (P＜0.01). There was marked upregulation of MIF expression on injured lung tissue. The number of cell expressed MIF＋ , ED1+ and MIF with ED1 showed a strong positive correlation with PaO2, PWI and histological changes. CONCLUSION: MIF may play a pivotal role in mediation of progressive lung injuries induced by intravenous oleic acid injection. In addition, the number of cells expressed MIF, especially macrophage, may reflect the severity of lung injury.  相似文献   

3.
AIM: To study the production of intercellular adhesion molecule-1(ICAM-1), E-selectin and P-selectin in serum, lung tissues and bronchoalveolar lavage fluid(BALF)of acute lung injury(ALI) model and to observe the effects of ambroxol combined with low-dose heparin on the changes of the 3 factors above.METHODS: Twenty-four healthy rabbits were randomly divided into 3 groups: normal saline control group (NC), oleic acid injury group (OA), ambroxol+ heparin treatment group (AH). The rabbit ALI model was induced by oleic acid injection through auricular vein. Partial pressure of O2 in artery(PaO2) was analyzed.The concentrations of ICAM-1 and E-selectin were detected by ELISA.The apoptosis index(AI) was measured by TUNEL method.The expression of P-selectin was determined by immunohistochemical method.The ultrastructural changes of the lung tissues were observed under electron microscope, and the lung wet/dry ratio(W/D) was calculated.RESULTS: PaO2 in AH group and OA group was significantly lower (P<0.01) than that in NC group, and PaO2 in AH group was significantly higher than that in OA group (P<0.01). The concentrations of ICAM-1 and E-selectin in serum, lung tissues and BALF, and AI and W/D in lung tissues in AH group were higher (P<0.05 or P<0.01) than those in NC group, and was lower than those in OA group (P<0.05 or P<0.01). In NC group, no significant change of the above parameters at all time points was observed (P>0.05). In OA group, PaO2 was significantly decreased (P<0.01) with the pathological process developed, and the concentrations of ICAM-1 and E-selectin were significantly increased. In AH group, PaO2 was decreased (P<0.05),and the concentrations of ICAM-1 and E-selectin were increased with the process of ALI developed. The P-selectin expression in lung tissues of OA group was distributed mainly in inflammatory cells, capillary endothelial cells and plasma. From low to high levels, the order was NC group < AH group < OA group in the expression of P-selectin. The most obvious apoptosis was observed in OA group. No apoptosis or occasional positive cells were found in NC group. The apoptotic rate in AH group was significantly reduced compared with that in OA group.CONCLUSION: In ALI induced by OA, ICAM-1, E-selectin and P-selectin are significantly increased and are involved in the occurrence and development of ALI. Ambroxol combined with low-dose heparin reduces the levels of ICAM-1, E-selectin and P-selectin, the pulmonary edema and the lung injury, improves pulmonary functions, and plays an important role in the prevention and treatment of acute lung injury.  相似文献   

4.
AIM:To observe the effects of the combination of positive end expiratory pressure (PEEP) and 80×10-6 nitric oxide (NO) inhalation on oleic acid induced acute lung injury (ALI) in canine.METHEDS:30 dogs were divided into 6 groups. Oleic acid was injected through Swan-Ganz catheter to induced ALI. Pulmonary and systemic hemodynamics,blood gas were measured in dogs before and after injection of oleic acid and the period of inhaled NO for 1-6 h. The methemoglobin(MHb) concentrations were measured. Histology and ultrastructure of the lung tissue were observed. RESULTS:(1) The combination of PEEP and 80×10-6 NO inhalation rapidly reduced mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance (PVR), increased PaO2/FiO2, reduced A-aDO2 without inducing significant change on systemic hemodynamics. Arterial blood levels of MHb did not change significantly. (2)The combination group was showed the lightest ALI change by HE stain and electron microscopy. CONCLUSION:The combination of PEEP and inhalation of 80×10-6 NO significantly and rapidly increased PaO2/FiO2 without producing lung injury induced by high FiO2 and high PEEP.  相似文献   

5.
AIM: To investigate whether hypercapnia is protective against acute lung injury (ALI) in a rabbit model, and study it's potential mechanisms. METHODS: Twenty-two healthy New Zealand white rabbits were involved in this study, and randomly allocated to control group (group C), normocapnic group (group N) and hypercapnic group (group H). Oleic acid (0.1 mL/kg) was injected intravenously to establish ALI model. Lung mechanics, hemodynamics, blood-gas analysis, the content of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissue were measured. Apoptosis was analyzed after 3h mechanical ventilation. RESULTS: (1) Peak airway pressure in group H was significantly lower than that in group N (P<0.05) and the dynamic lung compliance was significantly higher than that in group N (P<0.05). (2) PaO2 in group H was significantly higher than that in group N(P<0.05). (3) The content of MDA was significantly lower but the activity of SOD was significantly higher in group H than that in group N (P<0.05). (4) Apoptosis index in group H was significantly lower than that in group N (P<0.01). (5) Histologic damage was significantly severer in group N than group H. (6) PaCO2 was correlated with pH, PaO2, dynamic lung compliance, peak airway pressure and pulmonary permeability index (r=－0.928, P<0.01; r=0.511, 0.526, -0.506, -0.556, P<0.05, respectively). CONCLUSION: Hypercapnia protects lung from oleic acid-induced injury in rabbits. The mechanisms of protection might be associated with improvement of oxidation/anti-oxidation imbalance and inhibition of apoptosis.  相似文献   

6.
AIM:To approach the relationship between the expression of intercellular adhesion (ICAM-1 mRNA) and acute lung injury (ALI) as well as the mechanisms of rhubarb in the prevention and treatment of the lung injury. METHODS:ALI animal model was performed by Lipopolysaccharide (LPS). The rats were divided into 4 groups: LPS group, control group, rhubarb+LPS group and dexamethasone+LPS group. Histopathological examination and biological markers were measured for the lung specimens. Molecular hybridization method was used to determine the expression of ICAM-1 mRNA. RESULTS:The ICAM-1 mRNA expression in the lung tissues of LPS group significantly increased compared with control group (P＜0.01), rhubarb and dexamethasone had the action of decreasing the ICAM-1 mRNA expression (P＜0.05, P＜0.01); pathologic changes and the biological markers of ALI significantly decreased or ameliorated. CONCLUSION:The increase in the expression of ICAM-1 mRNA in the lung tissues of ALI is involved in the formation of ALI. Rhubarb and dexamethasone can ameliorate the lung damage, mechanism of which may be related to the inhibition of ICAM-1 mRNA expression.  相似文献   

7.
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8.
AIM: To evaluate the effects of different ventilation strategies on gas exchange and extravascular lung water during early stage of acute lung injury (ALI). METHODS: Upon the establishment of oleic acid-induced ALI (diagnostic standard: PaO2/FiO2 ≤ 300 mmHg), 24 adult mongrel dogs were randomly divided into 3 groups (n=8 each) according to different ventilation strategies: controlling high-concentration oxygen therapy (O2) group, continuous positive airway pressure (CPAP) group and bi-level positive airway pressure (BiPAP) group. The parameters of gas exchange and hemodynamics including the values of normal baseline, at ALI early stage (positive control) and from 1 to 4 h after treatment were recorded continuously. RESULTS: Compared with the value at the beginning of ALI, after 4 h of artificial ventilation, the improvement in oxygenation index (PaO2/FiO2) in BiPAP group (375.83±81.55, P<0.01) and CPAP group (327.17±78.82, P<0.01) were better than that in O2 group (255.00±49.85, P>0.05). The ratio of alveolar dead space to tidal volume [VD(alv)/VT]in O2 group further increased (P<0.01), while it obviously declined in CPAP group and BiPAP group (P<0.01). Oxygen delivery (DO2) in BiPAP group (P<0.01) was much higher than that in CPAP group and O2 group, while oxygen consumption (VO2) and oxygen extraction rate (O2ER) in O2 group were evidently higher than those in CPAP group and BiPAP group (P<0.05, P<0.01). After treatment, the alveolar-arterial oxygen differences [P(A-a)O2] of the 3 ventilation groups were significantly higher than the normal baseline values and the values at early ALI stage (P<0.01). BiPAP and CPAP greatly reduced the ratio of shunted blood to total perfusion (Qs/Qt) as compared with O2 group (P<0.01). Some parameters including pulmonary arterial wedge pressure (PAWP) and index of cardiac output (CI) kept stable, while mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance index (PVRI) further increased in CPAP group and BiPAP group (P<0.05,P<0.01). Three ventilation strategies did not effectively control the increase in extravascular lung water index (ELWI). CONCLUSION: During early stage of ALI, BiPAP and CPAP make active effects on improving gas exchange and tissue oxygenation. BiPAP displays more significant therapeutic effect than CPAP and oxygen therapy. The 3 ventilation strategies have no obvious effects on reducing extravascular lung water.  相似文献   

9.
AIM and METHODS: The protective effects of multi-enzyme Ⅱ was studied on cultured endothelial cells which was injuried by hyperlipidemia serum. RESULTS: Hyperlipidemia serum increased ICAM-1 expression on the surface of endothelial cells, and decreased NO2- release significantly (P＜0.01). ICAM-1 expression could be reduced and NO2- release could be enhanced markedly by multi-enzyme Ⅱ (P＜0.01). CONCLUSION: Multi-enzyme Ⅱ had an obvious protective effect on vascular endothelial cells which was injuried by hyperlipidemia seurm. Multi-enzyme Ⅱ could clean out oxide free radicals effectively because it had the acitive structure of both SOD and CAT.  相似文献   

10.
AIM: To determine the effects of recruitment maneuver(RM) strategy on oxygen metabolism and hemodynamics in canine models of extrapulmonary acut respiratory distress syndrome(ARDSexp) and pulmonary acute respiratory distress syndrome(ARDSp). METHODS: Twelve healthy canines were randomly divided into ARDSexp group and ARDSp group with 6 dogs each. To induce lung injury, the ARDSexp dogs were injected with oleic acid through femoral vein, and hydrochloric acid were administered by lung lavage to the ARDSp dogs. Pressure control ventilation (PCV) with lung protective ventilation strategy (LPVS) was employed to RM. Phigh was set to upper inflection point (UIP), and Plow was set to lower inflection point (LIP)+2 cmH2O.The duration of RM was 60 s and followed by baseline ventilatory settings. The indexes of oxygen metabolism and hemodynamics were measured before and after RM. RESULTS: After RM, arterial partial pressure of oxygen (PaO2), venous partial pressure of oxygen (PvO2), mixed venous oxygen saturation (SvO2) and oxygen delivery (DO2) obviously increased, and oxygen extraction ratio (ERO2) gradually decreased in both groups. PaO2, PvO2, SvO2 and DO2 in ARDSexp group were significantly higher than those in ARDSp group, and ERO2 in ARDSexp group were significantly lower than that in ARDSp group. Although mean pulmonary arterial pressure (MPAP), central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) significantly increased and mean arterial pressure (MAP) and cardiac index (CI) obviously decreased in both groups during RM, they reversed rapidly after RM. During RM, MPAP, CVP and PAWP were significantly higher, and MAP and CI were significantly lower in ARDSp group than those in ARDSexp group. CONCLUSION: RM increases oxygen delivery and improves tissue anoxia, and the better effects are obtained in ARDSexp dogs than those in ARDSp dogs. The effects of RM on hemodynamics are temporary and the ill effects are worse in ARDSp dogs than those in ARDSexp dogs.  相似文献   

11.
AIM:To study the effects of oxidized high-density lipoprotein (oxHDL) on the expression of monocyte chemoattractant protein-1(MCP-1) and intercellular adhesion molecule-1(ICAM-1) and intracellular free calcium concentration ([Ca2+]i) level in cultured human umbilical venous endothelial cells(HUVECs). METHODS:The MCP-1 protein content in the medium of conditioned HUVEC was measured by ELISA, and the ICAM-1 on HUVECs was detected by indirect immunofluorescence, and [Ca2+]i was determined by Fluo-3/AM, the injury of cells was observed by scanning electron microscopy (SEM).RESULTS:oxHDL could induce the expression of MCP-1 and ICAM-1 in HUVECs. In oxHDL group (HUVECs were incubated with 100 mg protein/L oxHDL for 24 h), the levels of MCP-1, ICAM-1 and [Ca2+]i increased by 160%, 60% and 70% respectively compared with the control group (P＜0.01). When HUVECs were incubated with 300 mg protein/L oxHDL for 24 h, cells were injured obviously. CONCLUSION:By inducing the expression of ICAM-1 and MCP-1 in endothelial cells, oxHDL may promote monocyte-endothelium adhesion and monocyte migration to intima, it may promote atherosclerosis as oxidized low-density lipoprotein (oxLDL).  相似文献   

12.
AIM:To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS:48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group(n=12), rats were bred 4 weeks;healthy control II group(n=12), rats were bred for 3months. (2) Model group I (n=12), 200μg lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method.RESULTS:The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups(P＜0.01,P＜0.05).FEV0.3/FVC% of two model groups, PaO2 and SaO2 of model I group were significantly decreased, while Ri and Re in model I group were significantly increased than that of control I group(P＜0.05). The PaCO2 and the counts of lymphocytes and alveolar macrophages of both model groups were significantly increased than those of the control groups (P＜0.01). Lots of alveolar macrophages had phagocyted smoke granules. The amounts of hydroxyproline of two model groups were significantly increased than those of control group((P＜0.05) and were negatively related to the FEV0.3/FVC%, respectively (P＜0.01,P＜0.01) and positively related to airway resistance of model I group(P＜0.01). CONCLUSIONS:COPD rat models were successfully established by passive cigarette smoking plus intratracheal instillation of LPS and cigarette smoking only. The pathologic changes were similar but milder than those of COPD patients. The airway obstruction of model I group was more severe than that of model II group, but they have no significant difference.  相似文献   

13.
AIM: To study the effects of colquhounia root tablet on the expression of adhesion molecule in acute lung injury of rats.METHODS: The rats were divided into 3 groups: ALI group,colquhounia root tablet＋ALI group and control group .ALI animal model was performed by treatment with oleic acid.The positive expression rates of CD11a,CD11b and CD18 in polymorphonuclear neutrophils and monocytes were analyzed by flow cytometry.ICAM-1 expression in lung tissue was determined by immunohistochemistry,histopathological examination and biological markers were measured from lung specimens.RESULTS: Colquhounia root tablet decreased the expression of CD11a,CD11b and CD18 in polymorphonuclear neutrophils and monocytes,and ICAM-1 in lung tissue (P<0.01),pathologic changes and the biological markers of ALI significantly ameliorated.CONCLUSION: The increase in the expression of CD11a/CD18 and CD11b/CD18 in polymorphonuclear neutrophils and monocytes,and expression of ICAM-1 in lung tissues of ALI may be involved in the formation of ALI.Colquhounia root tablet effectively ameliorates the lung damage,mechanism of which may be related to inhibition of adhesion molecule expression.  相似文献   

14.
AIM: To explore the possible changes in cell adhesion molecules and composition of complement activation in patients with acute myocardial infarction (AMI). METHODS: The expression of leukocyte CD18, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular-cell adhesion molecule-1 (sVCAM-1) and composition of complement activation (sC5b-9) concentrations of patients with AMI (67 cases), old myocardial infarction (OMI, 42 cases) and 38 healthy volunteers were measured using enzyme-linked immunosorbent assay(ELISA). RESULTS: The expression of leukocyte CD18, sICAM-1,sVCAM -1 and sC5b-9 were significantly higher in AMI patients than that in normal controls and OMI patients(P＜0.01). Interestingly, it was also found that the expression of leukocyte CD18, sICAM-1,sVCAM-1 and sC5b-9 concentrations were much higher in patients with ventricular arrhythemia (VA) and the died than that in patients without VA and survivals (P＜0.01). Furthermore, the leukocyte CD18 expression, sICAM-1 and sVCAM-1 were positively correlated to sC5b-9 in AMI patients (r=0.648,0.652,0.668,0.698,0.914,0.725,0.737,0.752,0.792,P＜0.01),and leukocyte CD18 expression was positively correlated to sICAM-1 and sVCAM-1(r=0.662,0.683,0.695,0.738,0.744,0.745, P＜0.01).CONCLUSION:The interaction of cell adhesion molecules and composition of complement activation might participate in the occurance and development of AMI,and closely related to the seriousness of patients'condition and prognosis.  相似文献   

15.
AIM：To investigate the effects of Xijiao Dihuang and Yinqiao San decoction (XDY) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in mouse lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) infected with influenza virus, and to explore its mechanism for treatment of viral pneumonia. METHODS：Fifty-four male BALB/c mice were randomly divided into normal group, model group and XDY group (n=18 in each group). The viral pneumonia model was established by intranasally dripping influenza A (H1N1) virus into the mice. The mice in XDY group were treated with XDY 1 h after dripping the virus. The expression of ICAM-1 and VCAM-1 in lung tissues was examined by immunohistochemical staining 2, 4 and 6 d after infection. On the other hand, RPMVECs were obtained from male Wistar rats and primarily cultured. The cells were randomly divided into control group, virus group, virus+XDY group, tumor necrosis factor α (TNF-α) group and TNF-α+XDY group. The mRNA and protein expression of ICAM-1 and VCAM-1 was evaluated by real-time PCR and flow cytometry 24 h after infection. RESULTS：Virus exposure increased ICAM-1 and VCAM-1 expression in mouse lung tissues (P<0.01), and XDY treatment attenuated this effect (P<0.01). Virus and TNF-α both led to the increases in mRNA and protein expression of ICAM-1 and VCAM-1 in RPMVECs (P<0.01), which were also reduced by treatment with XDY (P<0.01). CONCLUSION：Treatment with XDY decreases virus-induced ICAM-1 and VCAM-1 expression, suggesting an important role of XDY in treatment of viral pneumonia.  相似文献   

16.
AIM: To investigate the effects of non-ventilated lung with N2O on systemic oxygenation and lactic acid level in arterial blood during one lung anesthesia. METHODS: Twenty-two patients, ASA Ⅰ-Ⅲ, scheduled for selective pulmonary surgery, were randomly divided into two groups: control group (group A, n=11) and observation group (group B, n=11). Group A: the non-ventilated lung was kept open to the air; group B: N2O 2 cmH2O through CPAP system was insufflated into the non-ventilated lung during one lung ventilation. The anesthesia was induced with intravenous midazolam (0.05 mg·kg-1), propofol (0.5-1.0 mg·kg-1), fentanyl (4 μg·kg-1), and vecuronium (0.1 mg·kg-1) and was maintained with inhaling isoflurane. Blood gas analysis and lactic acid was recorded 20 min after two-lung ventilation (TLV) in the supine position, 20 min after one-lung ventilation (OLV) in the supine position, 20 min and 40 min after OLV in the lateral position and at the end of operation and the shunt fraction was calculated. RESULTS: PaO2 in group B was significantly higher than that in group A (P＜0.05). Qs/Qt in group B was significantly lower than that in group A (P＜0.05), and lactic acid level in group B was significantly lower than that in group A during OLV. CONCLUSION: Non-ventilated lung with N2O (2 cmH2O) improves systemic oxygenation, reduces intrapulmonary shunt and prevents hypoxemia during OLV.  相似文献   

17.
AIM:To evaluate the effect of pulmonary gas exchang and hemodynamic by inhaled nitric oxide on ischemia-reperfusion(I/R) lung in rabbit model.METHODS:Forty Newzealand rabbits were divided into four groups: group Ⅰ, sham-operated; group Ⅱ, sham-operated with inhaled nitric oxide (NO); group Ⅲ, I/R; group Ⅳ, I/R with Inhaled NO. Pulmonary artery pressure (PA), pulmonary vascular resistance(PVR), arterial oxygen tension(PaO2), arterial carbon dioxide tension (PaCO2), alveolar-arterial gradient (A-aDO2), Shunt fraction (Qs/Qt) expression of CD18, peripheral leukocyte, methemoglobin were continuetly quantitated. RESULTS:At the start of reperfusion inhaled NO significantly improved PaO2 and decreased PA, PVR,PaCO2,A-aDO2,Qs/Qt.CONCLUSION:Inhaled NO ameliorated significantly the early gas exchange and hemodynamic of reperfusion lung.  相似文献   

18.
AIM: To study the mechanism of protective effect of exogenous carbon monoxide (CO) in the lung injury induced by ischemia-reperfusion (IR) of hind limbs in rats. METHODS: Thirty-two SD rats were randomly divided into 4 groups: control, control+CO, IR and IR+CO. A rat model of ischemia in hind limbs and the reperfusion lung injury was made. The rats in IR+CO and control+CO groups were exposed to air containing 2.5×10-8 CO for 1 h before reperfusion or the corresponding control time point, while the other two groups were exposed to the routine air. The lung tissue structure, polymorphonuclear leukocyte (PMN) count, wet-to-dry weight ratio (W/D), malondialdehyde (MDA) content and the animal survival rate were observed. The carboxyhemoglobin (COHb) levels in artery blood were detected with CO-oximeter and the expression of intercellular adhesion molecule-1 (ICAM-1) in the lung was detected by Western blotting. RESULTS: Compared to control, the animal mortality, lung PMNs number, W/D, MDA content and ICAM-1 expression were all significantly increased in IR group. Compared with the IR group, the blood COHb level was significantly increased and the animal mortality, lung PMNs number, W/D, MDA content and ICAM-1 expression were all significantly decreased in IR+CO group. CONCLUSION: These data suggest that exogenous CO attenuate limb IR-induced lung injury by down-regulatiny ICAM-1 expression and suppressing PMN sequestration in the lung following limb IR in rats.  相似文献   

19.
AIM：To investigate the effects of rosiglitazone (ROSI),an agonist of peroxisome proliferator-activated receptor γ (PPARγ),on the lung expression of intercellular adhesion molecule-1 (ICAM-1) and cytokine-induced neutrophil chemoattractant (CINC) in rats with acute lung injury.METHODS：Thirty-six male Wistar rats were randomly divided into six groups：control group,ROSI group,GW9662 (a PPARγ antagonist) group,lipopolysaccharide (LPS,6 mg/kg,iv) group,ROSI-LPS group (0.3 mg/kg ROSI iv 30 min prior to LPS) and GW9662-ROSI-LPS group (0.3 mg/kg GW9662,iv,20 min before ROSI).Four hours after LPS injection,wet/dry weight (W/D) ratio,myeloperoxidase (MPO) activity,malondialdehyde (MDA) and CINC-1 concentrations were assayed in the lung tissues.Immunohistochemical analysis of ICAM-1 expression was also studied.RESULTS：Pretreatment with ROSI significantly attenuated LPS-induced increases in W/D ratio,MPO activity,MDA and CINC-1 concentrations as well as ICAM-1 expression in the lung tissues.The specific PPARγ antagonist GW9662 antagonized the effects of ROSI.CONCLUSION：Pretreatment with ROSI reduces LPS-induced lung injury in rats.The mechanism involves inhibition of the lung expression of ICAM-1 and CINC-1 by the activation of PPARγ.  相似文献   

20.
AIM: To investigate the effect of ischemic postconditioning (I-postC) on the expression of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in the lungs following intestinal ischemia reperfusion(II/R) in rats, and to explore the possible mechanism of I-postC in attenuating lung injury induced by II/R. METHODS: Thirty-two male Wistar rats were randomly divided into sham, II/R, intestinal ischemic postconditioning (II-postC) and limb ischemic postconditioning (LI-postC) groups. The model of intestinal I/R injury was established by clamping the super mesenteric artery for 45 min followed by 120 min of reperfusion in rats. At the end of the experiment, the changes of arterial blood gas and lung index were measured, and the morphological changes of the lung tissues were observed under light microscope. The content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) in the lung tissues were also detected. The contents of NF-κB p65 and ICAM-1 in lung tissue were determined by immunohistochemical staining and Western blotting. RESULTS: (1) Compared to those in II/R group, II-postC and LI-postC improved the respiratory functions of the lung, characterized by the increase in PaO2 and decrease in PaCO2 (P<0.05 vs II/R group). The lung index was decreased (P<0.01) and the pathologic lesion of the lung tissues was alleviated significantly by II-postC and LI-postC. (2) Both II-postC and LI-postC markedly inhibited the decrease in SOD activity, the increase in the content of MDA and the activity of MPO in the lung tissues (P<0.05 or P<0.01) induced by intestinal I/R. In addition, the over-expression of NF-κB p65 and ICAM-1 in the lung tissues was inhibited markedly by II-postC and LI-postC (P<0.05 or P<0.01 vs II/R group). CONCLUSION: I-postC attenuates lung injury induced by intestinal I/R in rats due to suppressing the activation of NF-κB and subsequent accumulation of neutrophils mediated by ICAM-1.  相似文献   

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