{'fraction_non_alphanumeric': 0.018556701030927835, 'fraction_numerical': 0.008934707903780068, 'mean_word_length': 4.894736842105263, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Acute Pancreatitis Is Not a Cause of Chronic Pancreatitis in the Absence of Residual Duct Strictures

It has been shown that intraductal injections of bile salts into the bile-pancreatic ducts of dogs or rats were immediately followed by acute hemorrhagic pancreatitis and, some months later, by persisting chronic pancreatitis. The study described in this article was designed to test the assumption that these chronic lesions were due to ductal strictures secondary to the toxic effect of bile salts. The bile-pancreatic ducts of 100 rats were injected with 0.2 ml of a solution containing 4 μM Na taurodeoxycholate and 0.2 μM trypsin. The 66 survivors were killed at intervals from 1 day to ± months following the induction of acute pancreatitis. Four to six sections were done in the first series, and serial 15-μM sections of the entire pancreas were taken from rats surviving ± months. These showed that from the sixth day on, the largest ducts draining pathological areas were obstructed by fibrosis. Distal to this obstruction, intralobular ducts were dilated and their epithelia flattened or atrophied. Acini were atrophied and replaced by peri- and intralobular fibrosis. Lesions were limited to areas drained by obstructed ducts, with the rest of the parenchyma being normal. We conclude that in experimental animals, as in human beings, chronic lesions that persist after acute pancreatitis are due to duct obstruction, not to acinar necrosis.