共查询到20条相似文献,搜索用时 15 毫秒
1.
Yang Chang Dong-hai Zhang Quan Hu Ling-ying Liu Yong-hui Yu Jia-ke Chai 《Burns : journal of the International Society for Burn Injuries》2018,44(4):905-916
Background
Burn–blast combined injury is a kind of injury caused by heat and blast at the same time. The lung injury after burn–blast combined injuries is of primary importance, and investigation of lung injury is needed in the clinical care of patients. Computed tomography (CT) is one of the standard tools used to observe the anatomical basis and pathophysiology of acute lung injury.Methods
We applied a method of fast 3D (three-dimensional) reconstruction to calculate the density value of the lung injury by CT analysis. Blast-injury group (BL group), burn-injury group (B group), burn–blast combined injury group (BBL group), and sham control group (C group) were established. Each group had 16 rats. The three-dimensional images of the lung tissue were obtained at 6 h, 24 h, and 48 h according to the CT value. The average density of the whole lung, left lung, and right lung were measured. The lung tissues were paraffin-embedded and HE stained. Smith scoring was performed according to the pathological findings.Results
In the BBL group, the density of the lung tissue was higher than those of the BL group and B group (P < 0.01). The lung tissue density values at 24 h after injury were higher than those at 6 h and 48 h after injury (P < 0.01). Pathological results confirmed the changes of density analysis of the lung tissue.Conclusion
The results have indicated that density analysis through a CT scan can be used as a way to evaluate lung injury in a burn–blast injury. 相似文献2.
3.
WUChang-yi ZENGYin-ming GUWei-dong DINGHao-zhong CHENXiao ZHANGYan 《国外医学:麻醉学与复苏分册》2004,25(4):240-243
Objective To investigate the role of moderate h.vpothennia in the lung inflammation of rat acute lung injury induced by lipopolysaccharide(LPS). Methods A rat model of acute lung injury (ALl) was established by in-tin-tracheal instillation of lipopolysaccharide ( 1.5 mg/kg, 0.5 ml) at 16 h after LPS ( 1.0 mg/kg) intraperitoneal adrninis-tmtion. Thirty-four male Sprague Dawley rats were randomly divided into four groups: control group, receiving saline only;LPS group, receiving LPS; hypothennia group, treated with hypothennia without LPS; LPS hypothennia group, treated with LPS and cooled to 32.5℃-33.0℃ as PaO2/FiO2. was below 300 mmHg. Hemodynamics and blood gases were record-ed every hour throughout the study. Rats were killed 4 h after ALl, and lung lavage was performed to measure the tumor ne-crosis factor α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) concentrations in bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). Results PaO2/FiO2 was significantly decreased and PaCO2 was increased in the LPS group as compared to their baseline values( P<0.01). Treatment with hypothermia inhib-ited the increase in PaCO2( P<0.05) but had no effect on PaO2/FiO2 in the presence of LPS. The administration of LPS significantly increased the concentrations of TNF-α, IL-6 and IL-10 in BALF as compared to the control experiment( P<0.05, P<0.01 ). Moderate hypothermia reduced the expressions of TNF-α and IL-6 ( P<0.01 ) but had no effect on the production of IL-10 ( P>0.05). Conclusion Moderate hypothermia significantly inhibits proinflammatory cytokine ex-pressions in lipopolysaccharide-induced acute lung injury. 相似文献
4.
《Burns : journal of the International Society for Burn Injuries》2020,46(4):762-770
ObjectiveVentilation strategies aiming at prevention of ventilator–induced lung injury (VILI), including low tidal volumes (VT) and use of positive end–expiratory pressures (PEEP) are increasingly used in critically ill patients. It is uncertain whether ventilation practices changed in a similar way in burn patients. Our objective was to describe applied ventilator settings and their relation to development of VILI in burn patients.Data SourcesSystematic search of the literature in PubMed and EMBASE using MeSH, EMTREE terms and keywords referring to burn or inhalation injury and mechanical ventilation.Study selectionStudies reporting ventilator settings in adult or pediatric burn or inhalation injury patients receiving mechanical ventilation during the ICU stay.Data extractionTwo authors independently screened abstracts of identified studies for eligibility and performed data extraction.Data synthesisThe search identified 35 eligible studies. VT declined from 14 ml/kg in studies performed before to around 8 ml/kg predicted body weight in studies performed after 2006. Low-PEEP levels (<10 cmH2O) were reported in 70% of studies, with no changes over time. Peak inspiratory pressure (PIP) values above 35 cmH2O were frequently reported. Nevertheless, 75% of the studies conducted in the last decade used limited maximum airway pressures (≤35 cmH2O) compared to 45% of studies conducted prior to 2006. Occurrence of barotrauma, reported in 45% of the studies, ranged from 0 to 29%, and was more frequent in patients ventilated with higher compared to lower airway pressures.ConclusionThis systematic review shows noticeable trends of ventilatory management in burn patients that mirrors those in critically ill non-burn patients. Variability in available ventilator data precluded us from drawing firm conclusions on the association between ventilator settings and the occurrence of VILI in burn patients. 相似文献
5.
Leyla Guler Murat Tavlasoglu Orhan Yucel Adem Guler Mehmet Ali Sahin Mustafa Kurkluoglu Yusuf Sirin Ayse Eken Mehmet Gamsizkan Mehmet Dakak Sedat Gurkok Onur Genc 《Journal of anesthesia》2014,28(3):347-353
Purpose
Taurine, the major intracellular free amino acid found in high concentrations in mammalian cells, is known to be an endogenous antioxidant and a membrane-stabilizing agent. It was hypothesized that taurine may be effective in reducing ischemia–reperfusion injury after lung transplantation and an experimental study was conducted in a rat model.Methods
The number of Sprague–Dawley rats used in the study was 35. Animals were randomized into five groups of 7 rats each, including control, donor I, donor II, ischemia–reperfusion injury, and treatment groups. All animals were exposed to the same experimental conditions in the preoperative period. Rats were fixed in a supine position after the induction. After the rats were shaved, a left pneumonectomy was performed following sternotomy in control, donor I, and donor II groups. The harvested grafts in donor I and donor II groups were transplanted to the rats of the ischemia–reperfusion group and treatment group, respectively. However, taurine was administered intraperitoneally for 3 days before the harvesting procedure in donor II. All harvested lungs were kept in a Euro-Collins solution at +4 °C for 24 h in a half-inflated manner. After harvesting and transplantation, lungs were sampled for histopathological and biochemical analysis.Results
Malondialdehyde and superoxide dismutase, glutathione peroxidase, and catalase levels were lower in the treatment group than the other groups (p < 0.05). Histopathological findings were better in treatment group than the ischemia–reperfusion group (p < 0.05).Conclusion
It was demonstrated that donor treatment with taurine resulted in preservation of transplanted lung tissue in respect to histopathological and biochemical findings. 相似文献6.
Chou-Chin Lan Chung-Kan Peng Shih-En Tang Hsueh-Ju Lin Sung-Sen Yang Chin-Pyng Wu Kun-Lun Huang 《The Journal of thoracic and cardiovascular surgery》2017,153(1):206-215
Objectives
Ischemia–reperfusion acute lung injury is characterized by increased vascular permeability, lung edema, and neutrophil sequestration. Ischemia–reperfusion acute lung injury occurs in lung transplantation and other major surgical procedures. Effective regulation of alveolar fluid balance is critical for pulmonary edema. Sodium-potassium-chloride co-transporter regulates alveolar fluid and is associated with inflammation. We hypothesized that sodium-potassium-chloride co-transporter is important in ischemia–reperfusion acute lung injury. Bumetanide, a sodium-potassium-chloride co-transporter inhibitor, is used to treat pulmonary edema clinically. We studied the effect of bumetanide in ischemia–reperfusion acute lung injury.Methods
Isolated perfusion of mouse lungs in situ was performed. The main pulmonary artery and left atrium were catheterized for lung perfusion and effluent collection for recirculation, respectively, with perfusate consisting of 1 mL blood and 9 mL physiologic solution. Ischemia–reperfusion was induced by 120 minutes of ischemia (no ventilation or perfusion) and reperfused for 60 minutes. Wild-type, SPAK knockout (SPAK?/?), and WNK4 knockin (WNK4D561A/+) mice were divided into control, ischemia–reperfusion, and ischemia–reperfusion + bumetanide groups (n = 6 per group). Bumetanide was administered via perfusate during reperfusion. Measurements were taken of lung wet/dry weight, microvascular permeability, histopathology, cytokine concentrations, and activity of the nuclear factor-κB pathway.Results
In wild-type mice, ischemia–reperfusion caused lung edema (wet/dry weight 6.30 ± 0.36) and hyperpermeability (microvascular permeability, 0.29 ± 0.04), neutrophil sequestration (255.0 ± 55.8 cells/high-power field), increased proinflammatory cytokines, and nuclear factor-κB activation (1.33 ± 0.13). Acute lung injury was more severe in WNK4 mice with more lung edema, permeability, neutrophil sequestration, and nuclear factor-κB activation. Severity of acute lung injury was attenuated in SPAK?/?mice. Bumetanide decreased pulmonary edema (wild-type: wet/dry weight 5.05 ± 0.44, WNK4: wet/dry weight 5.13 ± 0.70), neutrophil sequestration (wild-type: 151.7 ± 27.8 cells/high-power field, WNK4: 135.3 ± 19.1 cells/high-power field), permeability (wild-type: 0.19 ± 0.01, WNK4: 0.21 ± 0.03), cytokines, and nuclear factor-κB activation after ischemia–reperfusion.Conclusions
Functional reduction of sodium-potassium-chloride co-transporter by genetic or pharmacologic treatment to inhibit sodium-potassium-chloride co-transporter resulted in lower severity of acute lung injury induced by ischemia–reperfusion. Sodium-potassium-chloride co-transporter may present a promising target for therapeutic interventions in a clinical setting. 相似文献7.
Objective: To investigate the effect of pretreatment with Radix Paeoniae Rubra (RPR) on acute lung injury induced by intestinal ischemia/reperfusion in rats and its protective mechanism.
Methods: Thirty-two Wistar rats were randomly divided into four groups: Sham-operation group, ischemla/ reperfusion group (I/R group ), RPR-pretreatment group and hemin group. The model of intestinal ischemia/ reperfusion was established by clamping the superior mesenteric artery for 1 hour followed by 2-hour reperfusion. The effect of RPR on the expression of heme oxygenase-1 (HO-1) in lung tissues was detected by immunohistochemistry and morphometry computer image analysis. Arterial blood gas analysis, lung permeability index, malondialdehyde (MDA) and superoxide dismutase (SOD) contents in lungs were measured. The histological changes of lung tissue were observed under light microscope.
Resalts: The expression of HO-1 in RPR-pretreatment group and hemin group was obviously higher than that in sham-operation group and I/R group ( P 〈 0.01 ). The level of MDA and lung permeability index in RPR-pretreatment and hemin group were significantly lower than those in I/R group (P〈0.01 or P〈0.05), while the activity of SOD in RPR-pretreatment and hemin group was obviously higher than that in I/R group (P〈0.01). Under light microscope, the pathologic changes induced by I/R were significantly attenuated by RPR.
Conclusion: Intestinal ischemia/reperfusion may result in acute lung injury and pretreatment with RPR injection can attenuate the injury. The protective effect of RPR on the acute lung injury is related to its property of inducing HO-1 expression and inhibiting lipid peroxidation. 相似文献
Methods: Thirty-two Wistar rats were randomly divided into four groups: Sham-operation group, ischemla/ reperfusion group (I/R group ), RPR-pretreatment group and hemin group. The model of intestinal ischemia/ reperfusion was established by clamping the superior mesenteric artery for 1 hour followed by 2-hour reperfusion. The effect of RPR on the expression of heme oxygenase-1 (HO-1) in lung tissues was detected by immunohistochemistry and morphometry computer image analysis. Arterial blood gas analysis, lung permeability index, malondialdehyde (MDA) and superoxide dismutase (SOD) contents in lungs were measured. The histological changes of lung tissue were observed under light microscope.
Resalts: The expression of HO-1 in RPR-pretreatment group and hemin group was obviously higher than that in sham-operation group and I/R group ( P 〈 0.01 ). The level of MDA and lung permeability index in RPR-pretreatment and hemin group were significantly lower than those in I/R group (P〈0.01 or P〈0.05), while the activity of SOD in RPR-pretreatment and hemin group was obviously higher than that in I/R group (P〈0.01). Under light microscope, the pathologic changes induced by I/R were significantly attenuated by RPR.
Conclusion: Intestinal ischemia/reperfusion may result in acute lung injury and pretreatment with RPR injection can attenuate the injury. The protective effect of RPR on the acute lung injury is related to its property of inducing HO-1 expression and inhibiting lipid peroxidation. 相似文献
8.
Objective:To explore the relationship between neuronal apoptosis and hypoxia or traumatic injury.Methods:Rat neurons primarily cultured in vitro were treated with hypoxia (the hypoxia group) or traumatic injury (the trauma group).The neuronal apoptosis was evaluated with microscope,TUNEL (terminal deoxynucleotidyl transferase mediated x-dUTPnick end labeling) staining,flow cytometry,agarose get electrophoresis and immunohistochemistry.Results:Morphological changes of apoptosis appeared in the treated neurons,and the DNA fragmentation showed “ladder” break.The apoptotic index was 10.8% in the hypoxia group and 4.8% in the trauma group,while it was only 1.6% in the control group.The expression of apoptosis-associated genes(c-myc,fas and fasL) increased.Conclusions:Hypoxia or traumatic injury can induce neuronal apoptosis,and its molecular mechanism is probably related to the expressions of apoptosis-associated genes. 相似文献
9.
Li-Qun Mo Ye Chen Li Song Gang-Ming Wu Ni Tang Ying-Ying Zhang Xiao-Bin Wang Ke-Xuan Liu Jun Zhou 《The Journal of surgical research》2014
Background
Intestinal ischemia–reperfusion (II/R) is associated with high morbidity and mortality. The aim of this study was to investigate the effects of osthole on lung injury and mortality induced by II/R.Methods
A rat model of II/R was induced by clamping the superior mesenteric artery for 90 min followed by reperfusion for 240 min. Osthole was administrated intraperitoneally at 30 min before intestinal ischemia (10 or 50 mg/kg). The survival rate and mean arterial pressure were observed. Blood samples were obtained for blood gas analyses. Lung injury was assessed by the histopathologic changes (hematoxylin and eosin staining), lung wet-to-dry weight ratio, and pulmonary permeability index. The levels of reactive oxygen species, malondialdehyde, interleukin 6, and tumor necrosis factor α, as well as the activities of superoxide dismutase and myeloperoxidase in lung were measured.Results
The survival rate, ratio of arterial oxygen tension to fraction of inspired oxygen, and mean arterial pressure decreased significantly after II/R. Results also indicated that II/R-induced severe lung injury evidenced by increase in pathologic scores, lung wet-to-dry weight ratio, and pulmonary permeability index, which was accompanied by increases in the levels of pulmonary reactive oxygen species, malondialdehyde, interleukin 6, tumor necrosis factor α, and the pulmonary myeloperoxidase activity and a decrease in superoxide dismutase activity. Osthole could significantly ameliorate lung injury and improve the previously mentioned variables.Conclusions
These findings indicated that osthole could attenuate the lung injury induced by II/R in rats, at least in part, by inhibiting inflammatory response and oxidative stress. 相似文献10.
OBJECTIVE: To introduce a safe and specific approach of (13)C magnetic resonance spectrum ((13)C MRS) spectroscopy and investigate the alterations in hepatic anabolism. METHODS: Relative anaplerotic, pyruvate recycling and gluconeogenic fluxes were measured by (13)C MRS isotopomer analysis of blood glucose from rats with 40% body surface area burn injury, and from rats exposed to sham injury. A short chain fatty acid, [U (13)C] propionate which was avidly extracted by the liver, was infused intravenously to deliver (13)C into the citric acid cycle. Proton-decoupled (13)C MRS of deproteinized plasma or extracts of the freeze-clamped liver were used to determine the distribution of (13)C in blood or hepatic glucose. RESULTS: There was no difference in the multiplets detected in the glucose carbon-2 anomer from blood or liver after 45 or 60 minutes of the infusion of the propionate, indicating that steady-state isotopic conditions were achieved. Gluconeogenesis relative to citric acid cycle flux was not altered by burn injury; in both sham and burn groups the rate of glucose production was about equal to flux through citrate synthase. In the sham group of animals, the rate of entry of carbon skeletons into the citric acid cycle was about 4 times than that in the burn group. Similarly, flux through pyruvate kinase (again relative to citrate synthase) was significantly increased after the burn injury. CONCLUSIONS: Since results from analysis of the blood glucose are the same as that of the hepatic glucose, (13)C distribution in the glucose and hepatic metabolism can be assessed based on the (13)C MRS analysis of the blood glucose. 相似文献
11.
Ctodrlealbouiamdtea v.e1r rsAeumlsth acoirnuysgshta lamloaid ncy oren sstturuosdvcieietrassti iaholanv eisnu abtdhjdeerc aetscsu eotdefthat the relative benefits of albumin resuscitation,noconsensus has been reached by now.2Recently,theimmunomodulatory ef… 相似文献
12.
Paulo Thales Rocha de Sousa Ana Cristina Breithaupt-Faloppa Cristiano de Jesus Correia Raif Restivo Simão Sueli Gomes Ferreira Alfredo Inácio Fiorelli Luiz Felipe Pinho Moreira Paulina Sannomiya 《Journal of vascular surgery》2018,67(2):597-606
Objective
In surgical aortic repair or cardiac surgery with aorta occlusion, the occurrence of mesenteric ischemia and bowel injury has been associated with higher short-term mortality. The vascular protection of estrogens has been investigated and is mainly mediated by increasing the availability of nitric oxide (NO). Therefore, this study investigated the role of 17β-estradiol on visceral ischemia-reperfusion (I/R) injury after descending aorta occlusion in male rats.Methods
Mesenteric ischemia was induced in male Wistar rats by placing a 2F Fogarty arterial embolectomy catheter (Edwards Lifesciences, Irvine, Calif) in the descending aorta, which remained occluded for 15 minutes, followed by reperfusion for up to 2 hours. Rats were divided into four groups: (1) rats that underwent surgical manipulation only (sham, n = 22); (2) rats that underwent I/R injury (n = 22); (3) rats treated with intravenous 17β-estradiol (280 μg/kg) 30 minutes before I/R (n = 22); (4) or at the beginning of reperfusion (n = 22). Intestinal histopathologic changes were evaluated by histomorphometry. Mesenteric microcirculatory alterations were assessed by laser Doppler flowmetry and intravital microscopy technique. Protein expression of intercellular adhesion molecule-1, P-selectin, endothelial NO synthase (eNOS), and endothelin-1 was evaluated by immunohistochemistry; in addition, eNOS and endothelin-1 gene expressions were quantified by real-time polymerase chain reaction. Serum cytokines were measured by enzyme-linked immunosorbent assay.Results
Relative to the sham group, the I/R group exhibited a highly pronounced loss of intestine mucosal thickness, a reduction in mesenteric blood flow (P = .0203), increased migrated leukocytes (P < .05), and high mortality rate (35%). Treatment with 17β-estradiol before aorta occlusion preserved intestine mucosal thickness (P = .0437) and mesenteric blood flow (P = .0251), reduced the number of migrated leukocytes (P < .05), and prevented any fatal occurrence. Furthermore, 17β-estradiol downregulated the expression of intercellular adhesion molecule-1 (P = .0001) and P-selectin (P < .0001) on the endothelium and increased the protein expression of eNOS (P < .0001). The gene expressions of eNOS and endothelin-1 did not differ between the groups.Conclusions
The prophylactic treatment with 17β-estradiol showed better overall repercussions and was able to prevent any fatal occurrence, increase eNOS expression, thus preserving mesenteric perfusion and intestinal integrity, and reduce inflammation. 相似文献13.
Purpose
To establish a rat model of acute ischemic kidney injury by continually occluding the bilateral renal artery and renal veins, the functions of α-epithelial Na+ channel (α-ENaC) and aquaporin (AQP1) in lung injury induced by acute kidney injury (AKI) were examined and compared with lung injury induced by endotoxin.Methods
Male Wistar rats were randomly divided into three groups: control group, AKI group, and sepsis group. The concentrations of AQP1 and α-ENaC in the lung tissue were detected. The concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the serum and bronchoalveolar lavage fluid were also detected.Results
The arterial blood pH in AKI group and PaO2 in sepsis group decreased 2 h after the experiment. A significant pulmonary interstitial and alveolar space edema, which showed a typical pathological change in acute lung injury, was found in AKI and sepsis group 8 h after the experiment. Two hours after the experiment, the concentration of TNF-α and IL-6 in the serum and bronchoalveolar lavage fluid (BALF) in AKI and sepsis group increased, whereas the pulmonary expression of AQP1 and α-ENaC decreased. The pulmonary AQP1 and α-ENaC of the rats were negatively correlated with TNF-α and IL-6 in BALF. The relevance among AQP1, α-ENaC, TNF-α, and IL-6 in sepsis group was higher than that in AKI group.Conclusion
The TNF-α and IL-6 levels increased significantly and the pulmonary expression of AQP1 and α-ENaC declined at the early stage of AKI. 相似文献14.
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. 相似文献
15.
Changes in liquid clearance of alveolar epithelium after oleic acid-induced acute lung injury in rats 总被引:1,自引:0,他引:1
Impaired active fluid transport of alveolarepithelium may involve in the pathogenesis and resolution ofalveolar edema. The objective of this study was to explorethe changes in alveolar epithelial liquid clearance duringlung edema following acute lung injury induced by oleicacid. 相似文献
16.
Jaswinder Pal SinghAmrit Pal Singh MPharm Rajbir Bhatti MPharm 《The Journal of surgical research》2014
Background
Gallic acid is a polyphenolic compound and is reported to be renoprotective because of its antioxidant activity in various preclinical studies. Gallic acid has been reported to activate peroxisome proliferator–activated receptor gamma (PPAR-γ) in vitro. However, the relevance of the interplay between gallic acid and PPAR-γ in various pathologic conditions is yet to be established in vivo. The present study investigated the protective role of gallic acid against ischemia-reperfusion–induced acute kidney injury (AKI) and the possible involvement of PPAR-γ in gallic acid–mediated renoprotection.Materials and methods
The AKI was induced in rats through bilateral clamping of renal arteries for 40 min followed by reperfusion for 24 h. The AKI was assessed by the quantification of creatinine clearance, blood urea nitrogen, uric acid, potassium level, fractional excretion of sodium, and urinary microproteins. The oxidative stress in renal tissues was quantified in terms of myeloperoxidase activity, thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione level. The histopathologic changes in renal tissues were assessed by hemotoxylin and eosin staining. The rats were administered gallic acid (50, 100, and 200 mg/kg) orally for 7 d before subjecting them to AKI.Results
The renal ischemia–reperfusion induced significant changes in plasma, urinary, and tissue parameters. The administration of gallic acid at three dose levels offered a significant protection against renal ischemia-reperfusion–induced AKI. The prior treatment with PPAR-γ antagonist, bisphenol A diglycidyl ether, significantly abolished the renoprotective effect of gallic acid that confirms the involvement of PPAR-γ in gallic acid–mediated renoprotection.Conclusions
It is concluded that the activation of PPAR-γ significantly contributes toward gallic acid–mediated protection against ischemia-reperfusion–induced AKI. 相似文献17.
18.
Effect of terbutaline on alveolar liquid clearance after oleic acid-induced lung injury in rats 总被引:1,自引:0,他引:1
To investigate whether terbutaline affects alveolar liquid deorance after oleic acid-induced lung injury in rats. Methods : Forty healthy Wistor rats ( weighing 250- 280 g) were randomly divided into five groups ( n = 8 in each group ) : the normal control group ( control group ), oleic acid injury group (injury group), group (terbutaline group ), terbutaline plus amiloridetreated group ( terbutaline + amiloride group ) and terbutaline plus ouabaln-treated group (terbutaline + ouabaln group). Acute lung injury model was induced by intravenous oleic acid (0. 25 ml/kg body weight). 24 hours later, 1.5 μCi^125 I-labeled 5% albumin solution (5 ml/kg body weight) was dripped into the lungs through trachea. The alveolar liquid clearance rate, extravascular lung water content, and arterial blood gas were measured 1 hour thereafter. Results: At24 hours after infusion of oleic acid, the rats developed pulmonary edema and severe hypoxemia,with the alveolar liquid clearance rate decreased by 49. 2 % and the extravascnlar lung water content elevated by 47.9%. Compared with the rats in the injury group, terbutaline ( 10^-4 mol/L ) significantly increased the alveolar liquid clearance rate, decreased the extravascular lung water content and improved hypoxemia. The effect of terlmtaUne was partly blocked by amiloride and ouabain, which were inhibitors of sodium transport. Terbutaline increased the alveolar liquid clearance rate by 63.7 %, and amiloride and ouabain reduced the alveolar liquid clearance rate by 54.7 % and 56. 8 %, respectively. Conclusions: Terbutaline can accelerate alveolar liquid clearance through increasing sodim transport to attenuate pulmonary edema, thus improving gas exchange, which may have therapeutical effect on pulmonary edema after acute lung injury. 相似文献
19.