Reference : Transplantation pulmonaire et fonction mitochondriale
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Human health sciences : Cardiovascular & respiratory systems
Human health sciences : Surgery
http://hdl.handle.net/2268/23455
Transplantation pulmonaire et fonction mitochondriale
French
[en] Lung Transplantation and Mitochondrial Function
Detry, Olivier mailto [Centre Hospitalier Universitaire de Liège - CHU > > Chirurgie abdominale- endocrinienne et de transplantation >]
Willet, K. [> > > >]
Meurisse, Michel mailto [Université de Liège - ULg > Département des sciences cliniques > Chirurgicale abdominale]
Pincemail, Joël mailto [Université de Liège - ULg > > Chirurgie cardio-vasculaire >]
Limet, Raymond mailto [Université de Liège - ULg > Département des sciences cliniques > Chirurgie cardio-vasculaire et thoracique]
Sluse, Francis mailto [Université de Liège - ULg > Département des sciences de la vie > Bioénergétique et physiologie cellulaire >]
Defraigne, Jean-Olivier mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie générale]
2001
Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique
156
6, Pt 2
355-9
No
National
0377-8231
[en] The mechanisms of cellular lesions induced by lung ischemia and reperfusion are not fully understood and, in particular, the consequences of pulmonary ischemia and reperfusion injury on mitochondrial function have not been previously investigated. Therefore, we studied the respiratory function of isolated pulmonary mitochondria in a swine model of lung ischemia and reperfusion. We demonstrated that prolonged hypothermic (4 degrees C) ischemia induces significant lesions of the mitochondrial respiratory chain, particularly if ischemia is followed by normothermic reperfusion. These results should be integrated in the cellular alterations induced by the ischemia-reperfusion injury. In another swine model mimicking controlled non-heart beating donors, we demonstrated that thirty minutes of cardiac arrest do not promote significant alteration of the mitochondrial respiratory function. In contrast, forty-five minutes of cardiac arrest, induced significant mitochondrial lesions. This pulmonary tolerance to normothermic cardiac arrest might be explained by the presence of air in the lung airways, allowing some aerobic metabolism after circulatory arrest. These results suggested that lung grafts might be harvested from non-heart beating donors after thirty minutes of cardiac arrest, significantly increasing the pulmonary graft pool.
Researchers ; Professionals ; Students ; General public
http://hdl.handle.net/2268/23455

File(s) associated to this reference

Fulltext file(s):

FileCommentaryVersionSizeAccess
Restricted access
Bul.Acad.2001.pdfPublisher postprint6.94 MBRequest copy

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.