Chao 2018 J Burn Care Res
|Altered renal and cardiac mitochondrial activity after 40% TBSA in a swine model.|
Link: Open Access
Event: J Burn Care Res
Severe burn injury over 30% of the total body surface area (TBSA) leads to inflammation associated with organ damage. Acute kidney injury and altered cardiac function in this population further leads to poor recovery and increased mortality. Previous studies showed increased mitochondrial DNA and oxidative damage to mitochondria following severe burns. However, mitochondrial function in these organs following severe burns is not fully understood. The purpose of this study is to determine mitochondrial activity in the kidney and heart in a 40%TBSA burn swine model.
Seventeen anesthetized Yorkshire swine were subjected to 40% TBSA contact burn by brass probes. After 48 hours, heart and kidney tissues were harvested and analyzed by high-resolution respirometry. Citrate synthase (CS) enzyme activity analysis was performed, as well as western blots for mitochondrial fission and fusion proteins. Five non-burned swine served as control. Parametric and nonparametric t-tests were used, as appropriate, with significance at p<0.05.
Citrate synthase activity was significantly lower in burned swine kidney vs control (17.5 ± 1.7 vs 23.8 ± 3.6 nmol/s/ml, p<0.05), but not quite in heart. Maximal uncoupled respiration normalized to CS was significantly greater after burn in both hearts (616.5 ± 154.6 vs 254.1 ± 57.8 pmol O2/mg/s/CS activity, p<0.05, and kidneys (1067 ± 276.6 vs 590.2 ± 274.6 pmol O2/mg/s/CS activity, p<0.05), indicating less ATP generation. Mitochondrial efficiency to generate ATP was also significantly lower in burned swine kidney (61%) vs control (73%, p<0.05). Heart tissues also had significantly increased amounts of DRP1 post-burn (p<0.05) indicating greater mitochondrial fission from severe burns.
Severe burn injury results in altered mitochondrial activity and abundance in kidney and heart tissues. The burn-induced change in bioenergetics of heart and kidney is largely attributed to decreased mitochondrial abundance marked by increased mitochondrial fission. Additionally, mitochondria become less efficient in producing ATP due to increased uncoupled mechanisms.
The onset of mitochondrial dysfunction in heart and kidney tissues is seen as early as 48 hours post-burn injury. This may be an attractive therapeutic target to improve organ function and recovery in severe burns.
• Bioblast editor: Kandolf G
Labels: MiParea: Respiration, mt-Structure;fission;fusion, mt-Medicine
Organism: Pig Tissue;cell: Heart, Kidney
Coupling state: ET