Liver and skeletal muscle mitochondrial function following burn injury.
The possibility of altered mitochondrial function consequent to burn injury was investigated. Mitochondria isolated from liver or skeletal muscle of burn-injured rats (20% tbs) were compared at 3 days postburn to shams and normal controls. Mitochondrial yields were the same for all groups. ADP;O ratios were in the theoretical ranges expected and did not differ among burn, sham, and normal animals. Respiratory control ratios (RCR's) were decreased in liver mitochondria, averaging 71.7% of normal for burned animals compared to 95.8% for the sham group. The loss of respiratory control in liver mitochondria implies inefficient use of substrate chemical energy and could contribute to postburn hypermetabolism. The different response of muscle mitochondria as compared to liver suggests that alterations may be organ specific.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000378:metabolism*; D005971:Glutamates / Q000494:pharmacology; D006614:Hindlimb; D006885:Hydroxybutyrates / Q000494:pharmacology; D007656:Ketoglutaric Acids / Q000494:pharmacology; D008293:Malates / Q000494:pharmacology; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D008931:Mitochondria, Muscle / Q000378:metabolism*; D009243:NAD / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011773:Pyruvates / Q000494:pharmacology; D051381:Rats; D013386:Succinates / Q000494:pharmacology
D005971:Glutamates; D006885:Hydroxybutyrates; D007656:Ketoglutaric Acids; D008293:Malates; D011773:Pyruvates; D013386:Succinates; D009243:NAD; D000244:Adenosine Diphosphate