title: Peroxisomal fatty acid oxidation capacity is more resistant to ischaemic and reperfusion injury than mitochondrial fatty acid oxidation capacity in feline hearts.
abstract: We investigated ischaemic and postischaemic mitochondrial and peroxisomal fatty acid oxidation capacity, ATP levels and regional function in 40 anaesthetized open chest cats subjected to 10 or 40 min of regional myocardial ischaemia with or without 3 h of reperfusion (n = 10 in each situation). Following 10 min of ischaemia, the mitochondrial fatty acid oxidation capacity measured in tissue extracts from ischaemic tissue (nmol min-1 mg protein-1) was reduced in both subepi- and subendocardium, but was normalized in reperfused tissue extracts from both wall layers (0.29 +/- 0.03 and 0.30 +/- 0.04 vs. 0.57 +/- 0.05 and 0.59 +/- 0.05. P < 0.05). Peroxisomal fatty acid oxidation capacity in tissue extracts was unaffected by ischaemia and reperfusion. ATP levels and regional function measured in the LAD region was partly restored transmurally. After 40 min of LAD occlusion, mitochondrial fatty acid oxidation capacity was reduced, with higher activity in subepi- than in subendocardium (0.27 +/- 0.05 vs. 0.19 +/- 0.04. P < 0.05). Reperfusion did not restore mitochondrial fatty acid oxidation capacity. Peroxisomal fatty acid oxidation capacity was increased in the ischaemic subendocardium compared with levels in non-ischaemic subendocardium (0.53 +/- 0.02 vs. 0.45 +/- 0.03, P < 0.05), with normalization at the end of reperfusion. ATP levels were non-uniformly reduced during ischaemia and not repleted during reperfusion. Regional function recovered in circumferential segments but not in longitudinal segments following 40 min of ischaemia. In conclusion fatty acid oxidation enzymes seem to be more resistant to ischaemia in peroxisomes than in mitochondria. Mitochondrial fatty acid oxidation is fully reversible following shortlasting ischaemia, but remains depressed following prolonged ischaemia and reperfusion.
authors.affiliation: Department of Surgery, University of Bergen, Norway.
authors.forename: H
authors.initials: H
authors.lastname: Brunvand
authors.forename: L
authors.initials: L
authors.lastname: Frøyland
authors.forename: J
authors.initials: J
authors.lastname: Westby
authors.forename: E
authors.initials: E
authors.lastname: Hexeberg
authors.forename: R K
authors.initials: RK
authors.lastname: Berge
authors.forename: K
authors.initials: K
authors.lastname: Grong
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002415:Cats; D003326:Coronary Circulation / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D008830:Microbodies / Q000378:metabolism*; D008929:Mitochondria, Heart / Q000378:metabolism*; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D010084:Oxidation-Reduction
chemical_list: D000227:Adenine Nucleotides; D005227:Fatty Acids; D000255:Adenosine Triphosphate