Mechanisms of acute pancreatitis

Summary

Vascular mechanisms play an important but controversial role in the pathogenesis of acute pancreatitis. In experimental animals, injection of wax, powder, air, mercury, and microspheres into the pancreatic artery causes pancreatitis by end artery occlusion with resulting cellular infarction. Larger microspheres do not cause pancreatitis because collateral blood flow is preserved. Clinical evidence, such as microthrombi and atheromatous emboli in the pancreatic artery of patients with pancreatitis, supports pancreatic infarction as an etiologic agent. Experimental and clinical studies have suggested that pancreatic ischemia may also cause pancreatitis, but these studies have not been conclusive. We have compared five hours of total occlusion of the pancreaticoduodenal artery along with four hours of reperfusion to bile injection into the pancreatic duct as causes of pancreatitis. Bile injection caused a significant increase in serum amylase, activation of trypsin in pancreatic exudate, and histologic evidence of necrotizing pancreatitis. Pancreatic blood flow decreased as pancreatitis developed. Ischemia for five hours did not cause a significant increase in serum amylase or activation of trypsin in pancreatic exudate. Only edema was seen histologically, but there was no necrosis. Pancreatic blood flow increased with reperfusion. We believe ischemia aggravates, but does not initiate pancreatitis. Ischemia does not induce inflammation and necrosis in the pancreas, although infarction does.