To evaluate the in vivo effects of ischemia on the pancreas, 13 dogs had all blood vessels to the pancreas divided at laparotomy, except for the pancreatical duodenal artery and vein. In seven of the 13 dogs, ischemia was induced by clamping the pancreaticoduodenal artery for 5 h. In six dogs, pancreatitis was induced by injection of autologous bile (1 mL/kg body wt) into the pancreatic duct. Following ischemia or bile injection, the gland was reperfused and pancreatic blood flow was measured for the subsequent 4 h. Serum amylase was measured in all animals prior to operation, before arterial occlusion or bile injection, and after pancreatic perfusion. Pancreatic exudate was collected for trypsin assay. Gross and histologic examination of the pancreas and measurement of pancreatic water content was done on all specimens. Mean pancreaticoduodenal artery blood flow in ischemic animals showed reperfusion hyperemia immediately after removal of the arterial clamp, followed by a gradual return to baseline flow. Bile injection caused pancreatic blood flow to gradually decline to levels approximately one-half of baseline. Serum amylase rose significantly from baseline levels following bile injection (p<.05), but there was no significant change in serum amylase following 5 h of total ischemia and 4 h of reperfusion. Pancreatic water content increased with both ischemia and bile injection, but this increase reached statistical significance only with ischemia. Microscopically, edema was seen in the ischemic pancreas, but cellular architecture was preserved. Bile injection regularly revealed hemorrhage, necrosis, and disruption of acinar architecture. Trypsin activity was present in the exudate of four of six bile-injected dogs, but only one of seven ischemic dogs (p<.05).
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