Nickel carbonyl is a highly toxic metal compound produced from the reaction that occurs between nickel and carbon monoxide under pressure. As previously reported, nickel carbonyl can cause acute aspiration pneumonia, ...Nickel carbonyl is a highly toxic metal compound produced from the reaction that occurs between nickel and carbon monoxide under pressure. As previously reported, nickel carbonyl can cause acute aspiration pneumonia, and animal experiments showed it was toxic to animal lung, liver, brain, and other vital organs[1]. However, few studies have investigated nickel carbonyl poisoning in humans.展开更多
Patients with acute respiratory distress syndrome (ARDS) are currently treated with a lung protective ventilation strategy and the application of positive end-expiratory pressure (PEEP), sometimes in combination with ...Patients with acute respiratory distress syndrome (ARDS) are currently treated with a lung protective ventilation strategy and the application of positive end-expiratory pressure (PEEP), sometimes in combination with recruitment maneuvers. In this study, the respiratory system elastance and airway resistance of each breath before, during and after a specific recruitment maneuver (PEEP wave maneuver) were analyzed in two patient groups, ARDS and control group. A reduction of elastance after the maneuver was observed in ARDS patients. In addition, only healthy lungs exhibited a reduction of the elastance during the course of the maneuver, while the lungs of ARDS patients didn’t show that reduction of elastance. The capability of PEEP wave maneuvers to improve lung ventilation was shown and the dynamic behavior of the elastance after the maneuver was illustrated. Healthy lungs adapt faster to changes in mechanical ventilation than the lungs of ARDS patients.展开更多
Background Multiple organ dysfunction syndrome in the elderly （MODSE） is a problem with high mortality in the critical care of elderly patients. The pathogenesis of MODSE remains elusive. This study aimed to establi...Background Multiple organ dysfunction syndrome in the elderly （MODSE） is a problem with high mortality in the critical care of elderly patients. The pathogenesis of MODSE remains elusive. This study aimed to establish rat models of MODSE and to investigate the pathogenetic mechanism responsible for the development of MODSE in the rat models. Methods Twenty-four-month old rats （elderly） received intravenous injection of lipopolysaccharide （LPS） to induce rat model of MODSE. In the model, we observed the physical responses, biochemical indices changes, histopathological features of vital organs, including lung, liver, heart, and kidney. We also investigated the sequence of individual organ dysfunction and changes of proinflammatory factors. Three-month-old rats, serving as young rat controls, received parallel procedures. Besides, normal saline injection was also performed on elderly and young control rats. Results All rats displayed different degree of physical response after LPS injection, preceded by deterioration of respiratory status. At 6 hours, lung injury was observed, which started earlier than other organ injury that was observed in about 24 hours. Furthermore, all vital organ injury was more severe in elderly rats than in young rats at the same time points. After LPS injection, pulmonary alveolar macrophages apoptosis rate increased obviously, and was more significant in elderly rats （（43.4±8.4）%） than in young rats （（24.2±3.0）%）. LPS injection also enhanced tumor necrosis factor α （TNF-α） concentration significantly in these organs. Its peak concentration appeared at 6 hours in lung tissue and at 24 hours in other organs after LPS injection. TNF-α level was higher in elderly rats than in young rats at the same time points. The increase was most significant in lung tissue. After intravenous administration of LPS, toll-like receptor 4 （TLR4） expression in lung tissue was upregulated markedly, and peaked at 6 hours. In contrast, upregulation of TLR4 expression in liver peaked at 24 hours, lagging behind that in the lung. Conclusion Lung is the first and most seriously injured organ in rat model of MODSE and it may play an ＂initiating＂ role in the development of MODSE.展开更多
Mechanical ventilation (MV) is a dual blade sward which if misused could lead to lung injury, called ventilator induced lung injury (VILI). Pathogenesis of VILI is very complex with various manifestations, which is th...Mechanical ventilation (MV) is a dual blade sward which if misused could lead to lung injury, called ventilator induced lung injury (VILI). Pathogenesis of VILI is very complex with various manifestations, which is the focus in MV field in recent years. 1 In our research, the rats were ventilated with different tidal volume, then the pathological changes of the lungs were observed under macroscopy, light and electronic microscope, and various laboratory tests in blood and bronchoalveolar lavage fluid (BALF) were also carried out in order to probe further the pathologic characteristics and the pathogenesis of VILI.展开更多
Objective To observe the effect of Fuzheng Kang’ai Recipe(FKR)combined with gefitinib on the proliferation and apoptosis of lung cancer A549 cells,and to study its potential synergistic mechanish with gefitinib.Metho...Objective To observe the effect of Fuzheng Kang’ai Recipe(FKR)combined with gefitinib on the proliferation and apoptosis of lung cancer A549 cells,and to study its potential synergistic mechanish with gefitinib.Methods The effects of FKR(0.211,0.316,0.474,0.711,1.067,1.600,2.400,3.600 mg/mL)combined with展开更多
基金supported by the national "Tenth Five-year Plan" science and technology project (2001BA609A-19)
文摘Nickel carbonyl is a highly toxic metal compound produced from the reaction that occurs between nickel and carbon monoxide under pressure. As previously reported, nickel carbonyl can cause acute aspiration pneumonia, and animal experiments showed it was toxic to animal lung, liver, brain, and other vital organs[1]. However, few studies have investigated nickel carbonyl poisoning in humans.
基金Partial support by the EU-Project-“eTime”-ID:“FP7-PEOPLE-2012-IRSES”is gratefully acknowledged.
文摘Patients with acute respiratory distress syndrome (ARDS) are currently treated with a lung protective ventilation strategy and the application of positive end-expiratory pressure (PEEP), sometimes in combination with recruitment maneuvers. In this study, the respiratory system elastance and airway resistance of each breath before, during and after a specific recruitment maneuver (PEEP wave maneuver) were analyzed in two patient groups, ARDS and control group. A reduction of elastance after the maneuver was observed in ARDS patients. In addition, only healthy lungs exhibited a reduction of the elastance during the course of the maneuver, while the lungs of ARDS patients didn’t show that reduction of elastance. The capability of PEEP wave maneuvers to improve lung ventilation was shown and the dynamic behavior of the elastance after the maneuver was illustrated. Healthy lungs adapt faster to changes in mechanical ventilation than the lungs of ARDS patients.
文摘Background Multiple organ dysfunction syndrome in the elderly （MODSE） is a problem with high mortality in the critical care of elderly patients. The pathogenesis of MODSE remains elusive. This study aimed to establish rat models of MODSE and to investigate the pathogenetic mechanism responsible for the development of MODSE in the rat models. Methods Twenty-four-month old rats （elderly） received intravenous injection of lipopolysaccharide （LPS） to induce rat model of MODSE. In the model, we observed the physical responses, biochemical indices changes, histopathological features of vital organs, including lung, liver, heart, and kidney. We also investigated the sequence of individual organ dysfunction and changes of proinflammatory factors. Three-month-old rats, serving as young rat controls, received parallel procedures. Besides, normal saline injection was also performed on elderly and young control rats. Results All rats displayed different degree of physical response after LPS injection, preceded by deterioration of respiratory status. At 6 hours, lung injury was observed, which started earlier than other organ injury that was observed in about 24 hours. Furthermore, all vital organ injury was more severe in elderly rats than in young rats at the same time points. After LPS injection, pulmonary alveolar macrophages apoptosis rate increased obviously, and was more significant in elderly rats （（43.4±8.4）%） than in young rats （（24.2±3.0）%）. LPS injection also enhanced tumor necrosis factor α （TNF-α） concentration significantly in these organs. Its peak concentration appeared at 6 hours in lung tissue and at 24 hours in other organs after LPS injection. TNF-α level was higher in elderly rats than in young rats at the same time points. The increase was most significant in lung tissue. After intravenous administration of LPS, toll-like receptor 4 （TLR4） expression in lung tissue was upregulated markedly, and peaked at 6 hours. In contrast, upregulation of TLR4 expression in liver peaked at 24 hours, lagging behind that in the lung. Conclusion Lung is the first and most seriously injured organ in rat model of MODSE and it may play an ＂initiating＂ role in the development of MODSE.
文摘Mechanical ventilation (MV) is a dual blade sward which if misused could lead to lung injury, called ventilator induced lung injury (VILI). Pathogenesis of VILI is very complex with various manifestations, which is the focus in MV field in recent years. 1 In our research, the rats were ventilated with different tidal volume, then the pathological changes of the lungs were observed under macroscopy, light and electronic microscope, and various laboratory tests in blood and bronchoalveolar lavage fluid (BALF) were also carried out in order to probe further the pathologic characteristics and the pathogenesis of VILI.
文摘Objective To observe the effect of Fuzheng Kang’ai Recipe(FKR)combined with gefitinib on the proliferation and apoptosis of lung cancer A549 cells,and to study its potential synergistic mechanish with gefitinib.Methods The effects of FKR(0.211,0.316,0.474,0.711,1.067,1.600,2.400,3.600 mg/mL)combined with
