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Objective To study the influence of penehyclidine hydrochloride(PHC)on inflammatory factors in patients with acute lung injury(ALI).Methods Total of 96 patients with ALI were randomly divided into treatment group(48 cases)and control group(48 cases).Patients in the treatment group were given conventional therapy,plus penehyclidine hydrochloride injection 1 mg,im,q12 h or q8h,the first dose could be doubled,at least 2 days of continuous application;Patients in the control group were received conventional therapy.Tumor necrosis factor α (TNF-α),interleukin-6 (IL-6),high sensitive C reactive protein (hs-CRP),calcitonin (PCT),oxygenation index (PaO2/FiO2),lung injury score (LIS) and acute physiology and chronic health status score (APACHE II) of patients on each time point were compared between the two groups before and after treatment,and mechanical ventilation time,intensive care (ICU) treatment time,acute respiratory distress syndrome (ARDS) and ICU mortality were recorded.Results On each time point of treatment,TNF-α,IL-6,hs-CRP,PCT,LIS,APACHE II in treatment group were significantly lower than that of control group (P<0.05),PaO2/FiO2 was significantly higher than that of control group(P<0.01).The mechanical ventilation time,ICU treatment time in treatment group were shorter than that of control group(all P<0.05),The incidence of ARDS in treatment group and control group was 20.8% and 39.6%,respectively(P<0.05);ICU mortality rate was 12.5% and 31.2%,respectively(P<0.05).Conclusion Penehyclidine hydrochloride can effectively improve the oxygen metabolism in acute lung injury,regulate the pulmonary inflammatory response and improve the prognosis of patients.
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Objective To study the protective effect of nalmefene hydrochloride on lung ischemia-reperfusion injury and its mechanism.Methods 40 rats were randomly divided into model group,high dose of nalmefene group,low dose nalmefene group and sham operation group equally(n =10).The lung ischemia-reperfusion model was established by occlusion of the left pulmonary hilum.The intravenous injection of nalmefene (20,10 μg·kg-1) was applied at 10 minutes before occlusion of the left pulmonary hilum in the high dose of nalmefene group and the low dose of nalmefene group,respectively.The sham operation group without occlusion of the left pulmonary hilum was not given any treatment.At 2 h after reperfusion,all rats were detected arterial blood gas value and then sacrificed.The specimens from the upper lobe of the left lung tissue were preserved to observe pulmonary lesions,detect the ratio of wet / dry weight and the expressions of β-endorphin and interleukin(IL)-17.Results Compared with the model group,the value of PCO2,the degree of pulmonary lesions,the ratio of wet / dry weight and the expressions of β-endorphin and IL-17 in lung tissue were significantly decreased (P ＜ 0.01),while the value of PO2 was significantly increased (P ＜ 0.01) in the low dose of nalmefene group.Compared with the low dose of nalmefene group,thevalue of PCO2,the degree of pulmonary lesions,the ratio of wet/dry weight and the expressions of β-endorphin and IL-17 in lung tissue were significantly decreased (P ＜ 0.01),while the value of PO2was significantly increased (P ＜ 0.01) in the high dose of nalmefene group.Conclusion Nalmefene hydrochloride may prevent lung ischemia-reperfusion injury in a dose dependent manner by reducing the production of β-endorphin and inhibiting the expression of IL-17 in lung tissue.
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@#The characteristics of patients with spinal cord injury are shown as: disorder of the lung function and gas exchange, influence of body position, maximum inspiratory and expiratory pressure decreased, cough, airway obstruction, ect. The management of lung function currently include exercise, pacing therapy and medicine.
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Objective To study inhibition effect of rosiglitazone on lung injury induced by paraquat. Methods 72 male SD rats were randomly divided into three groups ( n=24 ): model control group, paraquat ( PQ ) was administered intraperitoneally at the dose of 20 mg·kg-1;rosiglitazone group, rosiglitazone (10 mg·kg-1 , ip) was administered 1 h before PQ administration; blank control group, 1 mL 0. 9% sodium chloride solution was administered intraperitoneally. The concentration of TNF-α and IL-1β in serum was measured by ELISA at 4, 8 h and 1, 3 day(s) after PQ exposure. The lung injury scores and nuclear factor-kappa B( NF-κB) positive signal were investigated 3 days after PQ exposure by HE staining and immunohistochemistry, respectively. Protein expression levels of NF-κB and activating protein-1(AP-1) were also determined by using Western blotting. Results The levels of IL-1β and TNF-α in serum of PQ-treated rats were significantly increased as compared with blank control group. Rosiglitazone pretreatment reduced the degree of lung tissue injury, the levels of IL-1β and TNF-α in serum, and the protien expression levels of NF-κB and AP-1 as compared with the model control group. Conclusion Rosiglitazone can inhibit NF-κB and AP-1 protein expression in lung tissue, reduce the levels of IL-1β and TNF-α in serum after PQ exposure, and exert an inhibition effect on inflammation in PQ-induced lung injury of rats.
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Objective To investigate the effect of resveratrol on levels of serum interleukin family of acute hemorrhagic shock patients and study its protective effect for secondary heart and lungs injury.Methods 42 cases of acute hemorrhagic shock were collected and divided into experimental group and control group according to different drugs treatment, each group had 21 cases.Control group were given continuous low flow oxygen, fluid infusion and other basic treatment, given blood transfusion if necessary.On the basis of control group, experimental group was given resveratrol 30 mg/kg, orally, one time per day for 4 consecutive weeks.The life index were detected during the treatment period.Then the levels of serum CK, LDH, IL-6, IL-10, IL-12, LVP, +dp/dtmax ,-dp /dtmax and arterial blood gas of all patients were detected after treatment.ResuIts Compared with control group, the levels of CK and LDH in experimental group decreased significantly (P<0.05);IL-6, IL-10, IL-12 levels decreased significantly (P<0.05).LVP,+dp /dtmax , -dp /dtmax level increased significantly ( P<0.05 ); PaCO2 and pH levels decreased significantly, the level of PaO2 increased significantly (P<0.05).ConcIusion Resveratrol can significantly reduce the serum IL-6, IL-10, IL-12l, reduce the CK, LDH level of hemorrhagic shock patients, and alleviate the injury of heart and lung.
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Objective To explore the inhibitory effect and possible mechanisms of lianhuaqingwen capsules on radiation-induced acute lung injury in rats. Methods Rats were randomly divided into control group, radiation group and radiation plus lianhuaqingwen group, the control group and the radiation group rats were given 0. 9% sodium chloride solution, the radiation plus lianhuaqingwen group rats were given lianhuaqingwen 0. 9% chlorine sodium solution. HE staining was applied to test the lung tissue inflammation; quantitative RT-PCR and ELISA were used to measure the content of IL-6, TNF-α and MCP-1 in rats;immunohistochemical assay was taken to detect the infiltration of macrophage in lung tissues. Results The relative mRNA expression of IL-6, TNF-α and MCP-1 in the control, radiation model control and radiation plus Lianhuaqingwen groups were (0. 002 1±0. 000 20),(0. 006 6±0. 000 32),(0. 003 9±0. 000 22); (0. 003 7±0. 000 16),(0. 007 4±0. 000 33),(0. 005 5± 0.000 24);(0.001 4±0.000 15),(0.005 4±0.000 72),(0.003 2±0.000 17),respectively; the concentration (pg·mL-1) of IL-6,TNF-αand MCP-1 in the serum were (35. 2±10. 9),(111. 8±26. 1),(68. 2±15. 2); (229. 3±28. 5),(837. 5±57. 6), (566. 9±39. 8);(96. 85±8. 20),(314. 53±12. 76),(191. 32±10. 97),respectively; and the macrophages at high magnification field in each group were (59. 5±4. 3),(503. 9±25. 8)and (106. 2±12. 6), respectively. Lianhuaqingwen capsules significantly alleviated the lung inflammation in rats with radiation-induced acute lung injury,inhibited the accumulation of macrophage in lung tissue,reduced the expression of IL-6 and TNF-α,and decreased the content of MCP-1 in lung tissues and sera(P<0. 05). Conclusion Lianhuaqingwen capsules attenuated the lung inflammation developed in rats with radiation-induced acute lung injury through inhibiting the expression of MCP-1 and reducing the accumulation of macrophage in lung tissues.
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Objective To investigate the protection mechanism of ulinastatin on bacterial endotoxin-induced acute lung injury. Methods Acute lung injury was induced by Escherichia colilipo-polysaccharide(LPS)5 mg·kg-1·d-1,intratracheally. Twenty SD rats were randomly divided into control group(n=10)and ulinastatin group(n=10). Ulinastatid group received ulinastatin 50 kU·kg-1 ,the control groups received the same amount of 0. 9% sodium chloride solution. Then the expression changes of rat AQP-1 and AQP-5,alveolar wall thickness change and the degree of pulmonary edema were detected. Results After the injection of LPS into the rat,the expression of AQP-1 and AQP-5 in control group were continuously decreased,but those in ulinastatin group decreased were not obvious. The lung wet/dry weight ratio in the control group increased significantly,the not obvious changes in the ulinastain group. The thickness of the alveolar in 24,48,72 h of the control group were(3. 84±0. 68),(6. 32±1. 08),(11. 03±2. 47)μm, respectively,and those in the ulinastian groups were(2. 31±0. 44)(,3. 76±0. 82)(,2. 94±0. 67)μm,respectively. Conclusion The AQP-1 and AQP-5 induced the occurrence of pulmonary edema by changing the cell permeability. Ulinastatin can slow down the process so as to reduce the degree of endotoxin-induced lung injury.
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Objective: To study the expression of L selectin and its possible role in pulmonary injury in rat models undergoing cardiopulmonary bypass (CPB) and to investigate the protecive effect of fucoidin during the procedure. Methods: Models of CPB and pulmonary perfusion in rats were used to investigate the expression of L selectin pre and post operation. Its expression in antagonist group was also studied. Other indexes, including the concentration of SOD, MDA and MPO in rat lung tissues as well as PaO 2/FiO 2 and histological changes, were studied to illustrate the possible mechanism of L selectin in lung reperfusion injury. Results: The expression of L selectin increased after creating CPB but decreased after pulmonary infusion with fucoidin during the procedure, and lung injury relieved as well. Conclusion: L selectin might lead to lung injury during CPB, blocking its expression may relieve lung injury and enhance the recovery of lung function.
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Objective To study the protective effects of bcl-2 gene against lung ischemia-reperfusion injury in vitro. Methods The lungs of rabbits were harvested respectively and preserved according to the way of lung transplantation. Then the lungs were reperfused using an ex vivo model. The rabbits were divided into 3 groups: control group, 0.9%NaCl was given; group2, Ad/Lac Z and group 3, receiving Ad/s-bcl-2. Agents were given to the rabbits by continuous intravenous infusion 48 hours before operations. Results Ad/s-bcl-2 increased the contents of bcl-2 mRNA in lung tissue, increased lung tissue SOD contents, decreased lung tissue MDA contents, decreased PAP, improved lung edema, reduced incidence of apoptosis and improved lung histological manifestation. These indexes in the Ad/s-bcl-2 group were better than in the groups of 0.9%NaCl and Ad/LacZ. Conclusion The bcl-2 gene amy provide significant protective effects on ischemia-reperfusion injury of the lung.
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Objective: To study the protective effect of anti-tumor necrosis factor-?antibody (TNF-? Ab) on lung injury after cardiopulmonary bypass(CPB). Methods: 20 patients with valve diseases underwent valve replacement under CPB. The patients were randomly divided into two groups: control group and TNF-? Ab group. In the TNF-? Ab group, human TNF-? Ab was dropped into the intracheal tube before operation and just after releasing the aortic clamp, respectively. Lung dynamic compliance, blood neutrophils count and TNF-? from the right and left atrium were determined perioperatively. Results: The dynamic compliance of the lung in TNF-? Ab group was higher than that in control group. TNF-? Ab can reduce releasing of TNF-? and restrain leukocyte accumulation in the lung. Conclusion: TNF-? Ab has markedly protective effect on lung injury after CPB.
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To ascertain whether heat shock gene expression could protect pulmonaryendothelial cell from hydrogen peroxide(H2O2)一indueed injury,the protective effect of HSPgene expression induced by pretreatment of bovine pulmonary endothelial eells(BPAECs)by heat shock (42 ℃, 2h)against lethal dose(lmmol?L(-1),45min) of H2O2一induced cyt-otoxieity was observed in vitro.It was found that BPAECs heat一shocked prior to exposureto H2O2(Immol?L(-1) 45min)showed significant decrease in H2O2一mediated incrementof LDH rdlease and TBARS production and had an obvious alleviation of H2O2一induccddecreased activities of catalase and superoxide dismutase. Further study showed thatcycloheximide, a protein synthesis inhibitor and Actinomycin D,a mRNA transcriptioninhibitor blocked the expression of HSP 70 and HSP 70 mRNA respectively.Both agentsprevented the cytoprotective effect of heat shock pretreatment against H2O2一mediatedBPAECs injury. The results suggested that HSP70 gene selectively translated after heat shockwas invoived in enhancement of eellular antioxidant mechanism and protected BPAECsagainst H2O2一induced injury
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10 adult female rats were used to study blast injuries of the air-way and lung. The conclusions are as follows. 1. There was significant difference in arterial blood gas analysis between the normal control and injury group. 2. The une-venness in the lung damage, bleeding, tear of the alveolar septa induced by the air shock wave was predominant, by scanning electron microscopy (SEM) as well as by the light microscopy (LM) . The bleeding may be due to the capillary rupture of alveolar septa. The' rope-like' structures seen might represent the fibre component in the septa which had more resistance to the local force and remained after the other components were wiped away by explosion. 3. Striping and fissure of the epithelium of trachea and bronchi of the injured group were detected. 4. The pathological changes observed with SEM were compared to those with LM.
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We observed the pulmonary responses and changes in TXB2 and 6-keto-PGF1a concentrations in plasma and lung lymph in endotoxin induced lung injury. The typical pulmonary responses appeared after the injury. The TXB2 concentrations in plasma and lung lymph increased by 24.5 and 30.7 times and those of 6-keto-PGFla by 10.6 and 15.7 times, respectively, as compared with baseline. The TXB2 and 6-keto-PGF1a concentrations in lymph were 68 and 75 percent higher than those in plasm a respectively. The results indicated that TXA2 and-PGI2 synthesis increased in the lung after injury and that TXA2 and PGI2 were important media in the lung injury.