The role of ischemia in acute pancreatitis: studies with an isolated perfused canine pancreas.

Recent clinical studies have suggested that ischemia may be an important factor in the pathogenesis of acute pancreatitis. The effects of ischemia on the pancreas were investigated utilizing the isolated perfused canine pancreas. Six control glands were perfused with autologous blood with an arterial Po2 ranging from 250 to 350 mm Hg. During the 4-hour perfusion period, gross appearance remained normal, weight gain was minimal (7 gm), and mean amylase levels (853 Caraway units [CU]/dl) remained within normal limits (less than or equal to 1,000 CU/dl). Lowering the arterial Po2 (range 30 to 60 mm Hg) in six glands while maintaining the flow at control levels elicited no significant change. Similarly, decreasing the flow (25% of control) with the arterial Po2 at 250 to 350 mm Hg produced no significant change in gross appearance, weight gain, or mean amylase levels. Combining low flow and low arterial Po2 in six glands also elicited no significant change as compared with controls. Four glands were subjected to total ischemia for 1 hour before being perfused. The glands became hyperemic, but mean weight gain (13 gm) and mean amylase levels (740 CU/dl) wee similar to those of controls. In contrast, in six glands subjected to total ischemia for 2 hours gross edema developed during the subsequent 4-hour perfusion. Mean weight gain (52 gm) and mean amylase levels (1,825 CU/dl) were significantly higher than in controls. These experimental data demonstrate that in the isolated perfused canine pancreas severe ischemia can produced significant injury. They therefore support the hypothesis that ischemia can clinically initiate acute pancreatitis.