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John H Dark - One of the best experts on this subject based on the ideXlab platform.
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early hemodynamic injury during donor Brain Death determines the severity of primary graft dysfunction after lung transplantation
American Journal of Transplantation, 2007Co-Authors: Vassilios S Avlonitis, Christopher Wigfield, Huw D R Golledge, J A Kirby, John H DarkAbstract:Sympathetic discharge and hypertensive crisis often accompany Brain Death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor Brain Death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain Death was induced by intracranial balloon inflation in rats, with or without α-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after Brain Death or sham procedure and reperfused using recipient rats. In a fourth group, Brain Death was induced and the lungs were retrieved 5 h after Brain Death and reperfused. Postreperfusion, lungs retrieved early from untreated Brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from Brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor Brain Death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.
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pulmonary transplantation the role of Brain Death in donor lung injury
Transplantation, 2003Co-Authors: Vassilios S Avlonitis, J A Kirby, A J Fisher, John H DarkAbstract:The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of Brain Death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of Brain Death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.
Vassilios S Avlonitis - One of the best experts on this subject based on the ideXlab platform.
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early hemodynamic injury during donor Brain Death determines the severity of primary graft dysfunction after lung transplantation
American Journal of Transplantation, 2007Co-Authors: Vassilios S Avlonitis, Christopher Wigfield, Huw D R Golledge, J A Kirby, John H DarkAbstract:Sympathetic discharge and hypertensive crisis often accompany Brain Death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor Brain Death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain Death was induced by intracranial balloon inflation in rats, with or without α-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after Brain Death or sham procedure and reperfused using recipient rats. In a fourth group, Brain Death was induced and the lungs were retrieved 5 h after Brain Death and reperfused. Postreperfusion, lungs retrieved early from untreated Brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from Brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor Brain Death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.
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pulmonary transplantation the role of Brain Death in donor lung injury
Transplantation, 2003Co-Authors: Vassilios S Avlonitis, J A Kirby, A J Fisher, John H DarkAbstract:The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of Brain Death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of Brain Death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.
Kathleen Mc Entee - One of the best experts on this subject based on the ideXlab platform.
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Lung expression of TNF-α and cytokines in Brain Death (BD)-induced lung injury.
2017Co-Authors: Asmae Belhaj, Laurence Dewachter, Sandrine Rorive, Myriam Remmelink, Birgit Weynand, Christian Melot, Emeline Hupkens, Céline Dewachter, Jacques Creteur, Kathleen Mc EnteeAbstract:Panel A. Relative lung mRNA expression of interleukin (IL)-6, IL-10, IL-1β, TNF-α and IL-8 at baseline, one (BD + 1 hour) and five (BD + 5 hours) hours after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and in the methylprednisolone-pretreated Brain Death (BD + Corticosteroids; n = 8; blue bars) groups. Panel B: Lung protein content for IL-6, IL-10 and IL-1β at baseline, one (BD + 1 hour) and five (BD + 5 hours) hours after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and in the methylprednisolone-pretreated Brain Death (BD + Corticosteroids; n = 8; blue bars) groups. Values are expressed as mean ± SEM. * p
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Mechanical versus humoral determinants of Brain Death-induced lung injury - Fig 7
2017Co-Authors: Asmae Belhaj, Laurence Dewachter, Sandrine Rorive, Myriam Remmelink, Birgit Weynand, Christian Melot, Emeline Hupkens, Céline Dewachter, Jacques Creteur, Kathleen Mc EnteeAbstract:Relative lung mRNA expression of intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM)-1 at baseline, one (BD + 1 hour) and five (BD + 5 hours) hours after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and in the methylprednisolone-pretreated Brain Death (BD + Corticosteroids group; n = 8; blue bars) groups. Values are expressed as mean ± SEM. * p
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Lung apoptosis in Brain Death (BD)-induced lung injury with and without methylprednisolone pretreatment.
2017Co-Authors: Asmae Belhaj, Laurence Dewachter, Sandrine Rorive, Myriam Remmelink, Birgit Weynand, Christian Melot, Emeline Hupkens, Céline Dewachter, Jacques Creteur, Kathleen Mc EnteeAbstract:Panel A. Pro-apoptotic Bax-to-Bcl-2 mRNA ratio at baseline, one (BD + 1 hour) and five (BD + 5 hours) hours after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and in the methylprednisolone-pretreated Brain Death (BD + Corticosteroids group; n = 8; blue bars) groups. Panel B. Lung apoptotic rate (percentage) was evaluated as the ratio between the numbers of the terminal deoxynucleotidyl transferase biotin-dUTP nick-end labelling (TUNEL)-positive cells (brown nuclei) and the total number of cells (brown + blue nuclei) at baseline and five hours (BD + 5 h) after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and in the methylprednisolone-pretreated Brain Death (BD + Corticosteroids group; n = 8; blue bars) groups. Illustrative microscopic TUNEL-immunostained lung sections (magnitude 400x) at baseline and at 5 hours after Cushing reflex in the BD and the BD + Corticosteroids treated pigs. Values are expressed as mean ± SEM. * p
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Mechanical versus humoral determinants of Brain Death-induced lung injury - Fig 3
2017Co-Authors: Asmae Belhaj, Laurence Dewachter, Sandrine Rorive, Myriam Remmelink, Birgit Weynand, Christian Melot, Emeline Hupkens, Céline Dewachter, Jacques Creteur, Kathleen Mc EnteeAbstract:Characterization of acute lung injury (Panel A) at baseline, one (BD + 1 hour) and five (BD + 5 hours) hours after Cushing reflex in the placebo-pretreated Brain Death (BD group; n = 11; red bars) and the methylprednisolone-pretreated Brain Death (BD + Corticosteroids; n = 8; blue bars) groups. Panel B: Correlations between the ratio PaO2/FiO2 and ALI score. Panel C: Illustrative microscopic views (magnitude 200x) of hematoxylin-eosin stained lung sections at baseline and at 5 hours after Cushing reflex in the BD and the BD+Corticosteroids treated pigs. Values are expressed as mean ± SEM., ‡ p
J Y Gauvrit - One of the best experts on this subject based on the ideXlab platform.
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revised ct angiography venous score with consideration of infratentorial circulation value for diagnosing Brain Death
Annals of Intensive Care, 2016Co-Authors: Antoine J Marchand, Philippe Seguin, Yannick Malledant, Marion Taleb, Helene Raoult, J Y GauvritAbstract:Background Computed tomography angiography (CTA) is largely performed in European countries as an ancillary test for diagnosing Brain Death. However, CTA suffers from a lack of sensitivity, especially in patients who have previously undergone decompressive craniectomy. The aim of this study was to assess the performance of a revised four-point venous CTA score, including non-opacification of the infratentorial venous circulation, for diagnosing Brain Death.
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revised ct angiography venous score with consideration of infratentorial circulation value for diagnosing Brain Death
Annals of Intensive Care, 2016Co-Authors: Antoine J Marchand, Philippe Seguin, Yannick Malledant, Marion Taleb, Helene Raoult, J Y GauvritAbstract:Computed tomography angiography (CTA) is largely performed in European countries as an ancillary test for diagnosing Brain Death. However, CTA suffers from a lack of sensitivity, especially in patients who have previously undergone decompressive craniectomy. The aim of this study was to assess the performance of a revised four-point venous CTA score, including non-opacification of the infratentorial venous circulation, for diagnosing Brain Death. A preliminary study of 43 control patients with normal CTAs confirmed that the infratentorial superior petrosal vein (SPV) was consistently visible. Therefore, 76 patients (including ten with decompressive craniectomy) who were investigated with 83 CTAs to confirm clinical Brain Death were consecutively enrolled between July 2011 and July 2013 at a university centre. The image analysis consisted of recording non-opacification of the cortical segment of the middle cerebral artery and internal cerebral vein (ICV), which were used as the reference CTA score, as well as non-opacification of the SPV. The diagnostic performance of the revised four-point venous CTA score based on the non-opacification of both the ICV and SPV was assessed and compared with that of the reference CTA score. The revised four-point venous CTA score showed a sensitivity of 95 % for confirming clinical Brain Death versus a sensitivity of 88 % with the reference CTA score. Non-opacification of the SPV was observed in 95 % of the patients. In the decompressive craniectomy group, the revised four-point CTA score showed a sensitivity of 100 % compared with a sensitivity of 80 % using the reference CTA score. Compared with the reference CTA score, the revised four-point venous CTA score based on ICV and SPV non-opacification showed superior diagnostic performance for confirming Brain Death, including for patients with decompressive craniectomy.
J A Kirby - One of the best experts on this subject based on the ideXlab platform.
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early hemodynamic injury during donor Brain Death determines the severity of primary graft dysfunction after lung transplantation
American Journal of Transplantation, 2007Co-Authors: Vassilios S Avlonitis, Christopher Wigfield, Huw D R Golledge, J A Kirby, John H DarkAbstract:Sympathetic discharge and hypertensive crisis often accompany Brain Death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor Brain Death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain Death was induced by intracranial balloon inflation in rats, with or without α-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after Brain Death or sham procedure and reperfused using recipient rats. In a fourth group, Brain Death was induced and the lungs were retrieved 5 h after Brain Death and reperfused. Postreperfusion, lungs retrieved early from untreated Brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from Brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor Brain Death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.
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pulmonary transplantation the role of Brain Death in donor lung injury
Transplantation, 2003Co-Authors: Vassilios S Avlonitis, J A Kirby, A J Fisher, John H DarkAbstract:The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of Brain Death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of Brain Death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.