Usage of density analysis based on micro-CT for studying lung injury associated with burn–blast combined injury

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.

Moderate hypothermia attenuates lung in flammation inlipopolysaccharide- induced acute lung injury in rats

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.     

Changes in ventilator settings and ventilation–induced lung injury in burn patients—A systematic review

ObjectiveVentilation strategies aiming at prevention of ventilator–induced lung injury (VILI), including low tidal volumes (V_T) 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. V_T 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.     

Taurine attenuates lung ischemia–reperfusion injury after lung transplantation in rats

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.     

Inhibition of Na-K-Cl cotransporter isoform 1 reduces lung injury induced by ischemia–reperfusion

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.

Protective effects of pretreatment with Radix Paeoniae Rubra on acute lung injury induced by intestinal ischemia/reperfusion in rats

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.     

Study on neuronal apoptosis induced by hypoxia or traumatic injury in rats

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.     

Osthole prevents intestinal ischemia-reperfusion–induced lung injury in a rodent model

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.     

Effect of burn injury on relative anaplerosis and gluconeogenesis in rats by ^13C magnetic resonance spectrum

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.     

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

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17β-Estradiol prevents mesenteric injury induced by occlusion of the proximal descending aorta in male rats

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.

Functions of aquaporin 1 and α-epithelial Na+ channel in rat acute lung injury induced by acute ischemic kidney injury

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.     

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.     

Changes in liquid clearance of alveolar epithelium after oleic acid-induced acute lung injury in rats

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.     

Explicit role of peroxisome proliferator–activated receptor gamma in gallic acid–mediated protection against ischemia-reperfusion–induced acute kidney injury in rats

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.     

Effect of terbutaline on alveolar liquid clearance after oleic acid-induced lung injury in rats

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.