THE ROLE OF ISCHEMIA IN ACUTE-PANCREATITIS - STUDIES WITH AN ISOLATED PERFUSED CANINE PANCREAS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 91  (4) , 377-382
Abstract
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 [partial pressure of O2] ranging from 250-350 mm Hg. During the 4-h perfusion period, gross appearance remained normal, wt gain was minimal (7 gm) and mean amylase levels (853 Caraway units [CU]/dl) remained within normal limits (.ltoreq. 1000 CU/dl). Lowering the arterial PO2 (range 30-60 mm Hg) in 6 glands while maintaining the flow at control levels elicited no significant change. Similarly, decreasing the flow (25% of control) with the arterial PO2 at 250-350 mm Hg produced no significant change in gross appearance, wt gain or mean amylase levels. Combining low flow and low arterial PO2 in 6 glands also elicited no significant change as compared with controls. Four glands were subjected to total ischemia for 1 h before being perfused. The glands became hyperemic, but mean wt gain (13 gm) and mean amylase levels (740 CU/dl) were similar to those of controls. In contrast, in 6 glands subjected to total ischemia for 2 h gross edema developed during the subsequent 4-h perfusion. Mean wt gain (52 gm) and mean amylase levels (1825 CU/dl) were significantly higher than in controls. In the isolated perfused canine pancreas severe ischemia can produce significant injury. Ischemia apparently can clinically initiate acute pancreatitis.