Acute respiratory distress syndrome(ARDS)is one of the most common severe diseases seen in the clinical setting.With the continuous exploration of ARDS in recent decades,the understanding of ARDS has improved.ARDS is ...Acute respiratory distress syndrome(ARDS)is one of the most common severe diseases seen in the clinical setting.With the continuous exploration of ARDS in recent decades,the understanding of ARDS has improved.ARDS is not a simple lung disease but a clinical syndrome with various etiologies and pathophysiological changes.However,in the intensive care unit,ARDS often occurs a few days after primary lung injury or after a few days of treatment for other severe extrapulmonary diseases.Under such conditions,ARDS often progresses rapidly to severe ARDS and is difficult to treat.The occurrence and development of ARDS in these circumstances are thus not related to primary lung injury;the real cause of ARDS may be the“second hit”caused by inappropriate treatment.In view of the limited effective treatments for ARDS,the strategic focus has shifted to identifying potential or high-risk ARDS patients during the early stages of the disease and implementing treatment strategies aimed at reducing ARDS and related organ failure.Future research should focus on the prevention of ARDS.展开更多
Background Polymorphonuclear neutrophil (PMN),one of the most important inflammatory cells,functions throughout the initiation,progression and resolution of inflammation. This study aimed at investigating the relation...Background Polymorphonuclear neutrophil (PMN),one of the most important inflammatory cells,functions throughout the initiation,progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma. Methods PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis,necrosis,survival and respiratory burst were detected by flow cytometry. Meanwhile,lactate dehydrogenase and (LDH) [Ca 2+ ]i were measured. Results The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma,and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile,lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control ( P <0.05) from 4 hours to 24 hours,and intracellular free Ca 2+ in PMN was increased temporarilly. Conclusions Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances,resulting in tissue injury. The temporary increase of intracellular free Ca 2+ may be responsible for the delayed apoptosis of PMN.展开更多
基金This study was supported by grants from the China Postdoctoral Science Foundation(No.2021T140794).
文摘Acute respiratory distress syndrome(ARDS)is one of the most common severe diseases seen in the clinical setting.With the continuous exploration of ARDS in recent decades,the understanding of ARDS has improved.ARDS is not a simple lung disease but a clinical syndrome with various etiologies and pathophysiological changes.However,in the intensive care unit,ARDS often occurs a few days after primary lung injury or after a few days of treatment for other severe extrapulmonary diseases.Under such conditions,ARDS often progresses rapidly to severe ARDS and is difficult to treat.The occurrence and development of ARDS in these circumstances are thus not related to primary lung injury;the real cause of ARDS may be the“second hit”caused by inappropriate treatment.In view of the limited effective treatments for ARDS,the strategic focus has shifted to identifying potential or high-risk ARDS patients during the early stages of the disease and implementing treatment strategies aimed at reducing ARDS and related organ failure.Future research should focus on the prevention of ARDS.
文摘Background Polymorphonuclear neutrophil (PMN),one of the most important inflammatory cells,functions throughout the initiation,progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma. Methods PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis,necrosis,survival and respiratory burst were detected by flow cytometry. Meanwhile,lactate dehydrogenase and (LDH) [Ca 2+ ]i were measured. Results The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma,and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile,lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control ( P <0.05) from 4 hours to 24 hours,and intracellular free Ca 2+ in PMN was increased temporarilly. Conclusions Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances,resulting in tissue injury. The temporary increase of intracellular free Ca 2+ may be responsible for the delayed apoptosis of PMN.
