ACINAR CELL RESPIRATION IN EXPERIMENTAL ACUTE-PANCREATITIS

The early pathogenetic steps that finally lead to acinar cell necrosis in acute pancreatitis have been characterized only scarcely as yet. A mong a lot of hypotheses, one concept favors disturbances of cellular energy metabolism as a major factor that contributes to preterm cell d ecline. To investigate, whether an experimental acute pancreatitis alt ers cell respiration, the respiratory capacities of acinar cells isola ted from rats with acute pancreatitis were measured. Acute pancreatiti s was induced using Popper's model, i.e., a combination of duct obstru ction, secretory stimulation, and mesenteric short-term ischemia with subsequent reperfusion. Acinar cells were isolated using a collagenase digestion technique. The respiratory rates of the isolated cells in s uspension were measured at 37 degrees C in 100% oxygen-saturated N-(2- hydroxyethyl)piperazine-N'-2-ethane acid-buffered Eagle's-minimal esse ntial medium. Resting respiration of the acinar cells uniformly amount ed to about 60 pmol of O-2/s x 10(6) cells in both the control and the pancreatitis group. Cellular respiration could significantly be stimu lated by stepwise uncoupling of oxidative phosphorylation by means of 2,4-dinitrophenol in all cell suspensions investigated. The maximum ra te of stimulated respiration was diminished in the cells isolated from rats with acute pancreatitis as compared with the controls (79.3 +/- 5.0 vs. 160.2 +/- 15.5 pmol of O-2/s x 10(6) cells, p <.05), however. This reduced respiratory load capacity of the acinar cells in acute pa ncreatitis reflects the restricted ability of the cells to increase re spiration on enhanced cellular demand. Since mitochondrial respiration is coupled to oxidative phosphorylation, an altered energy-transformi ng potential of the acinar cells in acute pancreatitis becomes evident . The data suggest that acute pancreatitis finds its reflection within the acinar cells themselves and that the capacity of the cells to adj ust respiration on enhanced demand under circumstances of acute pancre atic inflammation is disturbed.