Effects of bone marrow-derived mesenchymal stemcells engraftment on vascular endothelial cell growthfactor in lung tissue and plasma at early stage of smoke inhalation injury

BACKGROUND： This study was undertaken to determine the effect of mesenchymal stem cells （MSCs） engraftment on vascular endothelial cell growth factor （VEGF） in lung tissue, plasma and extravascular lung water at early stage of smoke inhalation injury.METHODS： A rabbit smoke inhalation injury model was established using a home-made smoke inhalation injury generator, and rabbits were divided into two groups randomly： a control group （S group, n=32） and a MSCs treatment group （M group, n=32）. 10 ml PBS was injected via the ear marginal vein immediately at injury into the S group. Third generation MSCs with a concentration of 1×107/10 ml PBS were injected via the ear marginal vein immediately at injury into the M group. VEGF in peripheral blood and lung tissue were measured at 0 （baseline）, 2, 4 and 6 hours after injection respectively and analyzed. The right lungs of rabbits were taken to measure lung water mass fraction.RESULTS： In the lung tissue, VEGF decreased gradually in the S group （P〈0.05） and signi？ cantly decreased in the M group （P〈0.05）, but it increased more signi？ cantly than the values at the corresponding time points （P〈0.05）. In peripheral blood, VEGF increased gradually in the S group （P〈0.05） and markedly increased in the M group （P〈0.05）, but it decreased more signi？ cantly than the values at corresponding time points （P〈0.05）.CONCLUSION： MSCs engraftment to smoke inhalation injury could increase VEGF in lung tissue, decrease VEGF in plasma and reduce extravascular lung water, indicating its protective effect on smoke inhalation injury.

Effects of early bronchoalveolar lavage fluid collected from dogs with smoke inhalation injury on the lungs of rats

Objective: Whether early massive bronchoalveolar lavage can remove the harmful substances from the lungs injured with smoke inhalation remains uncertain. This study was designed to observe the effects of early massive bronchoalveolar lavage fluid (BALF) on the healthy lungs in rats. Methods: Mongrel dogs were inflicted with severe smoke inhalation injury. The injured lungs were lavaged with large amount of normal saline in the first hour after injury and the BALF was collected. The BALF was injected into the healthy lungs of 30 rats (group C) in the dosage of 5 ml/kg. The functions and pathological changes of the lungs were observed 24 h after perfusion with the BALF. The data were compared with those of 23 rats (group B) whose lungs were perfused with the BALF collected from normal dogs and those of 21 rats (group A) whose lungs were perfused with normal saline. Results: The mortality rate 24 h after lung perfusion was higher in group C than in groups A and B. The survivors of group C exhibited fluctuation of respiratory rate (RR), remarkable decrease of PaO 2, significantly higher content of lung water, decrease of total static pulmonary compliance and pulmonary expansion index, and increasse of inflammatory cytokines in the tissues of lungs. Only slight mechanic obstructive effect on the airway was observed in rats of group A and B. The pathological changes of the lungs of the rats in group C were similar to those of the dogs with actual smoke inhalation injury. Conclusion: Our findings indicate that the BALF collected from dogs with acute severe smoke inhalation injury in the early stage after injury injured the normal lungs of rats with the bioactive substances in the BALF. These findings show us that it is a valuable therapeutic procedure to apply massive bronchoalveolar fluid lavage in the early stage after inhalation injury.

The Protective Effects of Preventive Atomisation Inhalation of Edaravone on the Lung Tissues of Rats with Smoke Inhalation Injury

Objective: To investigate the protective effects of the atomisation inhalation of edaravone on the lung tissues of rats with smoke inhalation injury. Methods: Forty male Sprague-Dawley (SD) rats were randomly divided into four groups of ten rats each: normal control group (group A), normal saline atomisation group (group B), edaravone aerosol group (group C) and edaravone atomisation prevention group (group D). Barring group A, the groups were used to create a model of severe smoke inhalation injury. However, before developing the model, group D rats were made to inhale edaravone (3.6 mg/mL) for 10 min. Six hours following smoke inhalation injury, abdominal artery blood samples were centrifuged, the lung tissue homogenate was prepared and carotid artery blood samples were used for blood gas analysis and oxygenation index (PaO2/FiO2) calculation. The levels of tumour necrosis factor alpha (TNF-α), interleukin (IL) 6 and IL-10 in serum and the levels of cysteine protease 3 (caspase-3), malondialdehyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) in lung tissues were examined. The wet-dry ratio (W/D) and water content of the lung tissue were calculated, and the TUNEL method was used to determine the rate of lung tissue apoptosis in each group. Tissue specimens were obtained from the partial lung for histopathological examination. Results: Compared with those in group A, the water content of the lung tissue, the rate of lung tissue apoptosis, W/D and the caspase-3, TNF-α, IL-6, IL-10, MDA and MPO levels were significantly greater in other groups (PP< 0.05). Compared with those in group B, the levels of W/D, the water content of the lung tissue, the rate of lung tissue apoptosis and the levels of caspase-3, TNF-α, IL-6, MDA and MPO were significantly low (P and the levels of IL-10, SOD and PaO2/FiO2 were significantly high in groups C and D (P The expression of the aforementioned factors was more evident in Group D (P < 0.05). Histopathological examination revealed that groups C and D had greater levels of inflammatory granulocytes than group B. This was more evident in group D. Conclusions: The inhalation of edaravone can reduce smoke inhalation-induced lung injury. This may be related to the inhibition of apoptosis, the reduction of peroxidation injury and the production/release of inflammatory mediators/free radicals. It exerts a remarkable preventive effect.

Effects of Cigarette Smoke Extract on E-cadherin Expression in Cultured Airway Epithelial Cells

Summary: To investigate whether the change of E-cadherin (ECD) expression plays a role in the injury and repair of airway epithelial cells (AEC) caused by smoking, porcine AECs were cultured by using an enzyme-dispersed method. After exposure of the AECs to cigarette smoke extract (CSE), the ECD expression in the cells was detected by using immunocytochemistry and in situ hybridization. The results showed that ECD was distributed on the plasma membrane at the cell junctions of AECs. After exposure to 20 % CSE, the membranous ECD expression was decreased, the cytoplasmic ECD expression was increased (P<0.01) as the exposure time went on. But the content of ECD mRNA in the AECs did not chang. It suggests that the change of ECD ex- pression is regulated at the posttranslational level and plays a role in the injury and repair of AEC caused by smoking.

Treatment of severe burn injury of 98%TBSA with 95% full-thickness burn and severe inhalation injury:a case report

The treatment of extensive severe burn injury is very difficult, especially when some complications are involved. A burned patient sustained 98% total body surface area (TBSA) with 95% full thickness burn and severe inhalation injury was admitted to our hospital in 08- 2000. After aggressive treatment, the patient recovered fully. This paper reports the treatment of the patient.

Serum zinc level is associated with liver dysfunction caused by white smoke inhalation

Background:White smoke bomb exposure in the military setting could result in organ injuries,which is uncommon and has been rarely described in previous studies.The aim of this study is to observe whether serum zinc levels are associated with liver function after white smoke inhalation.Methods:Fifteen patients with white smoke exposure were the subjects in this study.The clinical manifestations,liver function tests and the serum zinc levels were analysed.Results:The level of serum zinc was increased in the moderate or severe group(n=4)compared with that in the mild group(n=11).The four cases in the moderate or severe group had delayed impairment of liver function with an elevation of alanine transaminase.Additionally,increased blood concentrations of hyaluronic acid were found in three patients in the moderate or severe group.But no hexachloroethane or trichloropropane was detected.Conclusion:This study suggested that serum zinc levels may be associated with the severity of liver injuries after white smoke inhalation.

Influence of moxa smoke on mitochondrial transmembrane potential and Bax/Bcl-2 in alveolar type Ⅱ epithelial A549 cells

Objective： To investigate the influence of moxibustion products on mitochondrial transmembrane potential （MTP） and mRNA expression of Bax/Bcl-2 in alveolar type Ⅱ epithelial A549 cells, and to further explore influence of moxibustion products on the oxidative damage of A549 cells. Methods： Smoke and particles generated by moxibustion were collected using the filter box for gas sampling. The moxa smoke extract （MSE） was diluted sequentially to the final concentrations of 0.05 mg/mL, 0.2 mg/mL, 0.2 mg/mL, 0.3 mg/mL and 0.4 mg/mL using the cell culture medium, and A549 cells were then intervened by the above MSE solution. Cell MTP was detected by JC-1 staining. Fluorescence quantitative polymerase chain reaction （PCR） was used to detect Bax/Bcl-2 mRNA expression of A549 cells. Results： Compared with cells in the normal control group, MTP was significantly decreased in cells of 0.3 mg/mL and 0.4 mg/mL MSE intervention groups （P〈0.01）; while MTP showed no significant changes in cells of 0.05 mg/mL, 0.1 mg/mL and 0.2 mg/mL MSE intervention groups （P〉0.05）; compared with cells in 0.05 mg/mL MSE intervention group, MTP was decreased significantly in cells of 0.1 mg/mL, 0.2 mg/mL, 0.3 mg/mL and 0.4 mg/mL MSE intervention groups （P〈0.05）; compared with cells in 0.1 mg/mL MSE intervention group, MTP was decreased significantly in cells of 0.4 mg/mL MSE intervention group （P〈0.01）. Bax mRNA expression of cells in each concentration of MSE intervention group all showed no significant difference compared to that in the normal control group; Bcl-2 mRNA expression of cells was reduced with the increase of MSE intervention concentration. Wherein, Bcl-2 mRNA expressions of cells in 0.4 mg/mL and 0.3 mg/mL MSE intervention groups were significantly reduced compared with that of cells in the normal control group （P〈0.05）; Bcl-2 mRNA expression of cells in 0.4 mg/mL MSE intervention group was significantly reduced compared to that in 0.05 mg/mL MSE intervention group （P〈0.05）. Conclusion： Certain higher concentration of moxa smoke could reduce MTP and mRNA expression of the anti-apoptosis gene Bcl-2 in alveolar type Ⅱ epithelial A549 cells. Oxidative damage may be the important mechanism of apoptosis caused by the high concentration of moxa smoke solution, and further studies are necessary on the specific mechanisms.