Energy metabolism in rat pancreatic acinar cells during anoxia and reoxygenation.

Mitochondrial energy metabolism was studied in isolated pancreatic acinar cells during anoxia up to 90 min and reoxygenation for 60 min. To identify critical alterations leading to the known postanoxic impairments in structure and function of acinar cells, adenine nucleotide levels and the rates of phosphorylating and non-phosphorylating respiration were determined. ATP levels and the total amount of adenine nucleotides strongly decreased as early as after 30 min of anoxia. The cells partially restored ATP and the total adenine nucleotides within 60 min of reoxygenation. Long-term anoxia caused an increase in the oligomycin-insensitive part of oxygen consumption. The respiratory capacity measured as uncoupled respiration progressively declined to 40% of controls after 90 min of anoxia. Fluorescence measurements showed that flavoproteins and mitochondrial pyridine nucleotides in reoxygenated cells after short-term anoxia were in a more reduced state than in aerobic controls, and were not fully oxidizable by uncoupling. It is concluded that long-term anoxia produces an irreversible loss of respiratory capacity leading to a limited ATP production. This functional impairment and the progressive damage to acinar cells may be relevant for pancreatic injuries such as acute pancreatitis or post-transplantation pancreatitis.