Abstract
The light microscopic and ultrastructural changes seen in a canine model of chronic fibrosing pancreatitis are described. the distribution of the experimental lesion is similar to that of human chronic obstructive pancreatitis. the canine lesion is also compared to that of human chronic calcifying pancreatitis. It is suggested that the common denominator in all these conditions is an increased pressure in the terminal intercalated ducts which produces pressure atrophy of the acinar cells in the periphery of the obstructed lobules.