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Bugger, H; Chemnitius, JM; Doenst, T.
Differential changes in respiratory capacity and ischemia tolerance of isolated mitochondria from atrophied and hypertrophied hearts.
Metabolism. 2006; 55(8): 1097-1106. Doi: 10.1016/j.metabol.2006.04.005
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Führende Autor*innen der Med Uni Graz
Bugger Heiko Matthias

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In spite of opposing changes in rates of adenosine triphosphate turnover, hypertrophy and atrophy of the heart are accompanied by the same changes in gene expression, resembling a fetal genotype. Fetal hearts are characterized by increased ischemia tolerance. We assessed respiratory capacity of mitochondrial subpopulations from unloaded and pressure-overloaded hearts before and after 15 minutes of normothermic ischemia. Unloading was achieved by heterotopic rat heart transplantation and overloading by aortic banding. Respiratory chain gene expression (NADH dehydrogenase, cytochrome c oxidase [COX]) were analyzed by reverse transcriptase-polymerase chain reaction. Subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM) were isolated by differential centrifugation. Citrate synthase was used as mitochondrial marker enzyme. Adenosine diphosphate-stimulated oxygen consumption (state 3) was measured with a Clark-type electrode. Unloading resulted in atrophy, overloading in hypertrophy. State 3 was reduced in atrophied hearts both in SSM and IFM (SSM: 204 +/- 79 vs 804 +/- 147 natoms oxygen min(-1) mL(-1), P < .001; IFM: 468 +/- 158 vs 1141 +/- 296 natoms oxygen min(-1) mL(-1), P < .05), but was unchanged in hypertrophied hearts. NADH dehydrogenase and COX expression was also decreased with atrophy and was unchanged with hypertrophy. Ischemia caused decreased recovery of citrate synthase in isolates of SSM (P < .05) but not of IFM. State 3 in control hearts was reduced in IFM (-41%, P < .01) and SSM (-19%, not significant). This ischemia-induced decrease was less pronounced in SSM (-2%) and IFM (-22%) of atrophied and IFM (-23%) of hypertrophied hearts. Subsarcolemmal mitochondria of hypertrophied hearts displayed the greatest ischemia-induced decrease of state 3 (-32%, P < .05). In conclusion, (1) long-term changes in workload differentially affect maximal respiratory capacity and ischemia tolerance of isolated mitochondria. The changes are not parallel to the changes in energy requirements. (2) Mitochondria of atrophied hearts appear to be more resistant against ischemia than controls.
Find related publications in this database (using NLM MeSH Indexing)
Adenosine Diphosphate - metabolism
Adenosine Diphosphate - pharmacology
Animals -
Atrophy -
Body Weight - physiology
Cardiomegaly - metabolism
Citrate (si)-Synthase - metabolism
Cytochromes c - biosynthesis
Electron Transport - physiology
Gene Expression Regulation, Enzymologic - physiology
Heart Diseases - metabolism
In Vitro Techniques -
Male -
Mitochondria, Heart - metabolism
Muscle Proteins - biosynthesis
Myocardial Ischemia - metabolism
Myocardial Ischemia - physiopathology
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - physiopathology
NADH Dehydrogenase - metabolism
Organ Size - physiology
Oxygen Consumption - physiology
Rats -
Rats, Wistar -
Reverse Transcriptase Polymerase Chain Reaction -

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