AIMTo study the effect of ischemic preconditioning on lung injury following ischemia/reperfusion (I/R) in the hind limbs of rats.

METHODSWistar rats were randomly divided into four groups (n=8): control group,limbs ischemia/reperfusion (LI/R) group, ischemia preconditioning (IPC) group and L-NAME group. At the end of the experiment, blood/gas analysis and the contents of serum MDA, NO, ET and lung tissue MDA, NO, ET, MPO were measured. Meanwhile, lung index and W/D) of lung were measured.

RESULTSAfter the rats' hind limbs suffered ischemia/reperfusion, the level of PaO2 decreased and the values of W/D, LI, MPO of the lung issure and MDA, NO, ET of plasma and lung all increased significantly in the LI/R group; but the ratio of NO/ET decreased. Compared with LI/R group, the contents of NO and ratio of NO/ET increased but other parameters decreased in the IPC group. Compared with IPC group, the contents of NO and ratio of NO/ET decreased, but other parameters increased in the L-NAME group.

CONCLUSIONThe IPC can attenuate lung injury following IR in the hind limbs of rats, which may correlated with the increase of NO.

Acute Lung Injury ; prevention & control ; Animals ; Extremities ; blood supply ; Ischemia ; physiopathology ; Ischemic Preconditioning ; methods ; Lung ; blood supply ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; prevention & control

Radiation therapy is one of the main treatment methods for patients with thoracic malignant tumors, which can effectively improve the survival rate of the patients. However, radiation therapy can also cause damage to normal tissues while treating tumors, leading to radiation-induced lung injury such as radiation pneumonia and pulmonary fibrosis. Radiation-induced lung injury is a complex pathophysiological process involving many factors, and its prevention and treatment is one of the difficult problems in the field of radiation medicine. Therefore, the search for sensitive predictors of radiation-induced lung injury can guide clinical radiotherapy and reduce the incidence of radiation-induced lung injury. With the in-depth study of intestinal flora, it can drive immune cells or metabolites to reach lung tissue through the circulatory system to play a role, and participate in the occurrence, development and treatment of lung diseases. At present, there are few studies on intestinal flora and radiation-induced lung injury. Therefore, this paper will comprehensively elaborate the interaction between intestinal flora and radiation-induced lung injury, so as to provide a new direction and strategy for studying the protective effect of intestinal flora on radiation-induced lung injury.
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Humans ; Lung Injury/prevention & control* ; Gastrointestinal Microbiome ; Lung Neoplasms/radiotherapy* ; Lung/pathology* ; Radiation Injuries/metabolism* ; Thoracic Neoplasms

Burns and traumas are common injuries during both peace time and wartime. Lung is the earliest organ subjected to dysfunction and the incidence is highest. The systemic protective technology for the burn and trauma related lung injuries is based on evidence-based medicine and translational medicine. It includes a series of effective measures, such as rescue and treatment scheme for massive burn casualties, prophylactic tracheostomy, protective ventilation strategy, sequential cell protection, and prevention and treatment of sequelae, which prevents aggravation of lung injuries caused by ischemia reperfusion, oxidative stress, and iatrogenic factors, as well as reduces the incidence of complications to ensure the recovery after burns and traumas.
Burns ; complications ; Evidence-Based Medicine ; Humans ; Lung Injury ; etiology ; prevention & control ; Translational Medical Research

BACKGROUNDIt has found that ischemic postconditioning (IPO) might decrease pulmonary ischemia/reperfusion (I/R) injury, which is one of the main reasons of lung injury caused by cardiopulmonary bypass (CPB). It was found that aquaporins (AQPs) play a role in the maintenance of fluid homeostasis. But it is still unclear whether IPO influences the expression of aquaporin-1 (AQP1). This study was designed to investigate whether IPO can reduce CPB-related lung injury and affect the expression of AQP1 of lungs.

METHODSTwelve healthy dogs were divided into control group (C group) and ischemia postconditioning group (IPO group). CPB procedures were implemented. Ten minutes later, the left pulmonary artery was separated and blocked. Postconditioning consisted of two cycles of 5-minute pulmonary artery reperfusion/5-minute reocclusion starting at the beginning of reperfusion. The 2×4 cm tissues of both sides of pulmonary apex, superior, middle and inferior lobe were taken before CPB (T1), before occlusion and reopening of left pulmonary artery (T2, T3), and 2 hours after CPB (T4). Samples were used to evaluate lung injury degrees and to detect the expression of AQP1. At T1 and T4, blood was collected from femoral artery to calculate pulmonary function.

RESULTSAt T4, each pulmonary function showed significant deterioration compared with T1. Lung injury could be found at the onset of CPB. However, the expression of AQP1 decreased and wet to dry weight ratio (W/D) increased after T2. In the left lung of C group, the worst pulmonary function and structures were detected. The slightest changes were discovered in the right lung of C group. A close relationship between W/D and lung injury score was found. The lung injury score was negatively related with the expression of AQP1. It was found that the expression of AQP1 was negatively connected with W/D.

CONCLUSIONSIn dog CPB models, lung injury induced by CPB was related with down regulated expression of AQP1. AQP1 is believed to be involved in the mechanisms of lung ischemia/reperfusion (I/R) injury caused by CPB. IPO increases the expression of AQP1, provides a protective effect on lung suffering from CPB, and alleviates CPB-related lung injury.

Animals ; Aquaporin 1 ; metabolism ; Cardiopulmonary Bypass ; Dogs ; Humans ; Ischemic Postconditioning ; methods ; Lung Injury ; metabolism ; prevention & control ; Reperfusion Injury ; metabolism ; prevention & control

OBJECTIVE: To elucidate the pathogenic role of leukotriene B4 (LTB4) in pulmonary hyper-permeability and inflammation induced by lung-protective mechanical ventilation (LPMV) in rabbits. METHODS: Thirty-two healthy Japanese white rabbits were randomized into 4 groups for treatment with vehicle or bestatin (a leukotriene A4 hydrolase inhibitor that inhibits LTB4 production) administered intragastrically at the daily dose of 8 mg/kg for 5 days, followed by sham operation (group S and group BS, respectively, in which the rabbits were anesthetized only) or LPMV (group PM and group BPM, respectively, in which the rabbits received ventilation with 50% oxygen at a tidal volume of 8 mL/kg for 5 h). The concentrations of LTB4 and cyclic adenosine monophosphate (cAMP) in the lung tissues were analyzed by ELISA. cAMP content, protein kinase A (PKA) protein expression and the Rap1-GTP protein to total Rap1 protein ratio were determined to assess the activities of cAMP/PKA and Rap1 signaling pathways. The lung injury was evaluated by assessing lung permeability index, lung wet/dry weight ratio, polymorphonuclear leukocyte (PMN) count in bronchoalveolar lavage fluid (BALF), pulmonary myeloperoxidase (MPO) activity and lung histological scores. RESULTS: None of the examined parameters differed significantly between group S and group BS. All the parameters with the exception of lung histological score increased significantly in group PM and group BPM as compared to those in group S ( CONCLUSIONS LPMV can induce LTB4 overproduction to down-regulate cAMP/PKA and Rap1 signaling pathways in the lungs of rabbits, which results in lung hyper-permeability and inflammation. Bestatin can inhibit LTB4 production in the lungs to protect against LPMV-induced lung hyper-permeability and inflammation.
Animals ; Bronchoalveolar Lavage Fluid ; Leukotriene B4 ; Lung ; Lung Injury/prevention & control* ; Neutrophils ; Rabbits ; Respiration, Artificial/adverse effects*

To establish rat model of lung ischemia/reperfusion (IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 (MMP-9) and the possible mechanisms.
 Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group (S group), a IR group, and an experiment group (RA group) (n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide (PETCO2) reached 56-65 mmHg (1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry (W/D) and lung permeability index (LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured.
 Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion (both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group (P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group (both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly (both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group (P<0.01).
 Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.
Acidosis, Respiratory ; drug therapy ; prevention & control ; Animals ; Gene Expression Regulation, Enzymologic ; drug effects ; Lung ; enzymology ; Lung Injury ; enzymology ; Male ; Matrix Metalloproteinase 9 ; genetics ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; prevention & control

AIMOn the model of limb ischemia/reperfusion (LIR), the effects of taurine on pulmonary morphological changes in rats were observed.

METHODSWistar rats were divided into three groups (n=8): control group, ischemia/reperfusion group (IR) and taurine + IR (Tau + IR). Then macroscopic inspection and optical and transmission electron microscopies (TEM) were performed to assess the morphological changes of the lung tissues and their lung index (LI) and lung permeability index (LPI) and reactive oxygen species (ROS), malondialdehyde (MDA) were measured as well.

RESULTSThe morphological changes of lung tissue after LIR were characterized by an increase of permeability of the alveoli-capillary membrane and infiltration of inflammatory cells. Under optical microscopy, there were congestion and swelling in pulmonary microvessels with broadened the spaces around the blood vessels. Under TEM, a number of tight-junctional regions between adjacent alveolar epithelial cells and between pulmonary microvessels endothelium were "open". The LI, LPI, MDA and ROS increased. The specimens of Taurine + IR group revealed slight to moderate degrees of damages in the lung tissues.

CONCLUSIONTaurine protects lung from LIR in rats and the protective action on tight-junctional regions between cells and anti-oxygen is one of the protective mechanisms of taurine.

Animals ; Hindlimb ; blood supply ; Lung ; drug effects ; pathology ; Lung Injury ; prevention & control ; Male ; Malondialdehyde ; analysis ; Rats ; Rats, Wistar ; Reactive Oxygen Species ; analysis ; Reperfusion Injury ; prevention & control ; Taurine ; pharmacology ; Tight Junctions ; metabolism

Animals ; Cardiopulmonary Bypass ; Dogs ; Female ; Isoflurane ; pharmacology ; Lung ; blood supply ; Male ; Random Allocation ; Reperfusion Injury ; prevention & control

OBJECTIVETo study the protective effects of Ginkgo biloba extract (EGb) on the lung injury of dogs undergoing hypothermic cardiopulmonary bypass (CPB).

METHODSFourteen healthy hybrid dogs were randomly divided into the control group and the EGb group, 7 in each group. EGb (8 mg/kg) was intravenously dripped to dogs in the EGb group before thoracotomy after anesthesia, while equal volume of normal saline was intravenously dripped to those in the control group. The lung tissue was collected after 60-min CPB and 120-min recovery of heart beat. The lung tissues were collected to detect the wet weight-dry weight ratio and the permeability. The contents of malondialdehyde (MDA), the activities of myeloperoxidase (MPO) and total superoxide dismutase (T-SOD) in the lung tissues were detected by biochemical assay. The levels of IL-1beta, IL-8, tumor necrosis factor alpha (TNF-alpha), platelet activating factor (PAF) in the lung tissue were detected by enzyme linked immunosorbent assay (ELISA).

RESULTSCompared with the control group, the wet weight-dry weight ratio was reduced and the permeability of the lung tissue decreased (P < 0.05), the MDA content was reduced, the activity of MPO decreased, and the activity of T-SOD increased (P < 0.05), and the levels of IL-1beta, IL-8, and PAF obviously decreased (P < 0.05).

CONCLUSIONSEGb showed better protective effects on the lung injury of dogs undergoing hypothermic CPB. Its possible mechanisms might be associated with alleviating ischemia-reperfusion injury of in vitro circulation and systemic inflammatory response.

Animals ; Cardiopulmonary Bypass ; adverse effects ; methods ; Dogs ; Ginkgo biloba ; Lung Injury ; etiology ; prevention & control ; Plant Extracts ; pharmacology

Animals ; Hindlimb ; blood supply ; Intestine, Small ; metabolism ; Ischemia ; metabolism ; prevention & control ; Ischemic Preconditioning ; Lung Injury ; metabolism ; Male ; Muscle, Skeletal ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism