Báo cáo y học: " The role of poly (ADP-ribose) polymerase in ventilator-induced lung injury"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: The role of poly (ADP-ribose) polymerase in ventilator-induced lung injury. | Available online http content 12 5 431 Letter The role of poly ADP-ribose polymerase in ventilator-induced lung injury Michiel Vaneker Leo MA Heunks Johannes G van der Hoeven and Gert Jan Scheffer Department of Anesthesiology Radboud University Nijmegen Medical Centre PO Box 9101 6500 HB Nijmegen The Netherlands Corresponding author Michiel Vaneker Published 22 October 2008 This article is online at http content 12 5 431 2008 BioMed Central Ltd See related research by Kim et al. http content 12 4 R108 Critical Care 2008 12 431 doi ee7030 With interest we have read the paper by Kim and colleagues reporting the role of poly ADP-ribose polymerase PARP in ventilator-induced lung injury VILI in healthy mice 1 . Some issues have not been addressed appropriately. The authors show increased levels of TNFa in lung homogenate after 2 hours of lung-protective ventilation LPV . Previous data from our laboratory have shown in the healthy mouse lung that so-called protective mechanical ventilation tidal volume 8ml kg peak airway pressure 10 to 12cmH2O positive end-expiratory pressure 4 cmH2O induces a pulmonary inflammatory response 2 . In addition to elevated levels of TNFa we found increased expression of IL-1P IL-6 and keratinocyte-derived chemokine in the lung homogenate and found an increased number of pulmonary leucocytes in mice mechanically ventilated for 2 hours. Electron microscopy revealed evidence for type I pneumocyte membrane disrup tion and endothelial detachment indicating structural injury. In line with the findings by Kim and colleagues the wet dry ratio was not affected after 2 hours of mechanical ventilation -although in our study 4 hours of protective ventilation did increase the wet dry ratio. The so-called LPV-induced pulmonary inflammation can therefore occur without activation of PARP. It is possible that initiation of inflammation precedes the activation of PARP. Do the authors have any

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