The recovery of total DNA content and recovery of total cytochrome c oxidase activity in the rat liver after partial hepatectomy is accelerated by triiodothyronine applied in three doses, two before and one immediately after liver resection. Triiodothyronine-treated animals already have higher cytochrome c oxidase activity before resection. The recovery of the tissue oxidative capacity after partial hepatectomy is more rapid in triiodothyronine-treated animals. These data indicate that hormonal activation of the liver regeneration process is involved.
Ample experimental evidence suggests that sepsis could interfere
with any mitochondrial function; however, the true role of
mitochondrial dysfunction in the pathogenesis of sepsis-induced
multiple organ dysfunction is still a matter of controversy. This
review is primarily focused on mitochondrial oxygen consumption
in various animal models of sepsis in relation to human disease
and potential sources of variability in experimental results
documenting decrease, increase or no change in mitochondrial
respiration in various organs and species. To date, at least three
possible explanations of sepsis-associated dysfunction of the
mitochondrial respiratory system and consequently impaired
energy production have been suggested: 1. Mitochondrial
dysfunction is secondary to tissue hypoxia. 2. Mitochondria are
challenged by various toxins or mediators of inflammation that
impair oxygen utilization (cytopathic hypoxia). 3. Compromised
mitochondrial respiration could be an active measure of survival
strategy resembling stunning or hibernation. To reveal the true
role of mitochondria in sepsis, sources of variability of
experimental results based on animal species, models of sepsis,
organs studied, or analytical approaches should be identified and
minimized by the use of appropriate experimental models
resembling human sepsis, wider use of larger animal species in
preclinical studies, more detailed mapping of interspecies
differences and organ-specific features of oxygen utilization in
addition to use of complex and standardized protocols evaluating
mitochondrial respiration.