Abstract
Background: Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease, characterized by unexplained hypertrophy of the left ventricle. HCM features similar clinical and pathological characteristics in human beings and cats and is a common cause of sudden death and heart failure. Mitochondrial dysfunction and oxidative stress are well known to play a role in the development of various cardiovascular diseases. However, their roles in HCM remain unexplored.
Objectives
Methods: Cardiac muscle was obtained from eight cats diagnosed with naturally-occuring HCM (5 males; 2-10 years old, 6.3 ± 2.4 (mean ± SD)) and from nine age-matched control cats (CON) (3 males; 2-11 years, 4.9 ± 3.1). High-resolution respirometry was used to measure mitochondrial function in permeabilized, cardiac muscle fibres. Oxidative stress was assessed by measurements of mitochondrial H2O2 generation and thiobarbituric acid reactive substances (TBARS).
Results: In heart muscle of HCM cats, complex-I-linked state 3-respiration was significantly decreased (30 ± 16 pmol s -1 mg-1) compared to CON (64 ± 26 pmol s -1 mg-1) (P=0.006). Fatty acid oxidation with palmitoyl-carnitine and octanoyl-carnitine was significantly decreased in HCM hearts (12 ± 5 pmol s -1 mg-1) and (15 ± 4 pmol s -1 mg-1) compared to CON (28 ± 8 pmol s -1 mg-1) and (42 ± 16 pmol s -1 mg-1), respectively (P=0.0004). Mitochondrial H2O2 generation during state 3, with complex I-linked substrates, was significantly higher in HCM hearts compared to CON (P<0.05). TBARS in heart tended to be increased in HCM cats compared to CON.
Conclusion: Findings of the study indicate that mitochondrial dysfunction and enhanced oxidative stress may play an important role in the pathogenesis of feline HCM in the occult stage of disease.
Objectives
Methods: Cardiac muscle was obtained from eight cats diagnosed with naturally-occuring HCM (5 males; 2-10 years old, 6.3 ± 2.4 (mean ± SD)) and from nine age-matched control cats (CON) (3 males; 2-11 years, 4.9 ± 3.1). High-resolution respirometry was used to measure mitochondrial function in permeabilized, cardiac muscle fibres. Oxidative stress was assessed by measurements of mitochondrial H2O2 generation and thiobarbituric acid reactive substances (TBARS).
Results: In heart muscle of HCM cats, complex-I-linked state 3-respiration was significantly decreased (30 ± 16 pmol s -1 mg-1) compared to CON (64 ± 26 pmol s -1 mg-1) (P=0.006). Fatty acid oxidation with palmitoyl-carnitine and octanoyl-carnitine was significantly decreased in HCM hearts (12 ± 5 pmol s -1 mg-1) and (15 ± 4 pmol s -1 mg-1) compared to CON (28 ± 8 pmol s -1 mg-1) and (42 ± 16 pmol s -1 mg-1), respectively (P=0.0004). Mitochondrial H2O2 generation during state 3, with complex I-linked substrates, was significantly higher in HCM hearts compared to CON (P<0.05). TBARS in heart tended to be increased in HCM cats compared to CON.
Conclusion: Findings of the study indicate that mitochondrial dysfunction and enhanced oxidative stress may play an important role in the pathogenesis of feline HCM in the occult stage of disease.
| Original language | Danish |
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| Publication date | 16 May 2013 |
| Number of pages | 1 |
| Publication status | Published - 16 May 2013 |
| Event | at annual Phd Day at Faculty of Health and Medical Sciences - Panum Institute, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen, Denmark Duration: 16 May 2013 → 16 May 2013 |
Seminar
| Seminar | at annual Phd Day at Faculty of Health and Medical Sciences |
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| Location | Panum Institute, Faculty of Health and Medical Sciences, University of Copenhagen |
| Country/Territory | Denmark |
| City | Copenhagen |
| Period | 16/05/2013 → 16/05/2013 |