ORBi: Detry Olivier - Transplantation pulmonaire et fonction mitochondriale

Reference : Transplantation pulmonaire et fonction mitochondriale


	Document type :	Scientific journals : Article
	Discipline(s) :	Life sciences : Biochemistry, biophysics & molecular biology Human health sciences : Cardiovascular & respiratory systems Human health sciences : Surgery
	To cite this reference:	http://hdl.handle.net/2268/23455

Title :	Transplantation pulmonaire et fonction mitochondriale
Language :	French
Alternative title :	[en] Lung Transplantation and Mitochondrial Function
Author, co-author :	Detry, Olivier [Centre Hospitalier Universitaire de Liège - CHU > > Chirurgie abdominale- endocrinienne et de transplantation >]
	Willet, K. [> > > >]
	Meurisse, Michel [Université de Liège - ULg > Département des sciences cliniques > Chirurgicale abdominale]
	Pincemail, Joël [Université de Liège - ULg > > Chirurgie cardio-vasculaire >]
	Limet, Raymond [Université de Liège - ULg > Département des sciences cliniques > Chirurgie cardio-vasculaire et thoracique]
	Sluse, Francis [Université de Liège - ULg > Département des sciences de la vie > Bioénergétique et physiologie cellulaire >]
	Defraigne, Jean-Olivier [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie générale]
Publication date :	2001
Journal title :	Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique
Volume :	156
Issue/season :	6, Pt 2
Pages :	355-9
Audience :	National
ISSN :	0377-8231
Abstract :	[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.
Target :	Researchers ; Professionals ; Students ; General public
Permalink :	http://hdl.handle.net/2268/23455

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