Enhancement of mitochondrial function in sepsis

K. L. Dawson, E. R. Geller and J. R. Kirkpatrick
Department of Surgery, Wayne State University School of Medicine, Detroit.

Recent reports from our laboratory have challenged the concept that sepsis selectively damages or interferes with mitochondrial function. To address the lingering skepticism that mitochondrial assays in surviving animals might not detect this "injury," we injected rats with a lethal dose of Escherichia coli endotoxin and compared hepatic, cardiac, and skeletal muscle mitochondrial function in these animals with that of control rats. Mitochondrial function was serially determined during a four-hour postmortem period by measuring the respiratory control ratio, the adenosine diphosphate-oxygen ratio, and protein levels. Hepatic mitochondria ceased to function within 30 minutes of the time of death. Cardiac and skeletal muscle mitochondria functioned normally up to four hours after death in both septic and control animals. Mitochondria from septic animals had a significantly higher respiratory control ratio than those from control rats. Thus, sepsis appears to enhance rather than damage mitochondrial function up to four hours after death.