Very little is known about the pathogenesis of acute pancreatitis. Therefore, treatment consists primarily of supportive and symptomatic care. Many disorders and clinical situations are known to initiate episodes of acute pancreatitis. These include alcohol intake, gall stones, and ischemia. Exact pathogenetic mechanisms by which these stimuli cause pancreatitis, however, are unknown. Utilizing the ex-vivo, isolated, perfused canine pancreas model, experimental pancreatitis can be initiated by a variety of stimuli simulatilng clinical situations. Alcoholic hyperlipemic pancreatitis can be simulated in this preparation by infusing oleic acid (FFA) into the arterial line. Gall stone pancreatitis can be simulated by partially obstructing the pancreatic duct and maximally stimulating the gland. Ischemic pancreatitis can be induced in this preparation by a period of total ischemia before the perfusion is started. In all three of these instances the first physiologic change in the pancreas is an increase in capillary permeability. The pancreatitis can be modified or abated by the addition of an osmotically active agent, such as albumin. Furthermore, this capillary injury appears to be mediated at least in part, by oxygen-derived free radicals. By studying the pathogenetic pathways of experimental pancreatitis in this isolated organ model, it is hoped that effective treatment can be derived. A clinical trial evaluating the use of nasogastric suction in acute pancreatitis will be continued, and a clinical study evaluating albumin administration in severe acute pancreatitis will be initiated.
