{'fraction_non_alphanumeric': 0.023629489603024575, 'fraction_numerical': 0.000945179584120983, 'mean_word_length': 5.921568627450981, '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}}
[Centrolobular cholestasis: experimental study on the possible mechanism (author's transl)].

In the cholestatic condition of many different aetiologies a common pathologic picture is found. It is characterized by the presence of pigmented "plugs" and cytoplasmatic "masses" in the centrolobular region. Dubin has tried to interpret this on purely hydrostatic ground but this is not a very likely explanation. We tried to comprove this hypothesis studying the interference of a previous, or concomitant, centrolobular alteration in the distribution, morphology and intensity of cholestatic lesions: terminal choledochus ligatures were performed in animals intoxicated with carbon tetrachloride, a substance that damages predominantly the centrolobular region. In 6 dogs, terminal choledochus ligature was associated with carbon tetrachloride intoxication. A histological examination of the liver showed that the degree of centrolobular cholestasis was in the inverse ration of hepatocytic damage intensity. This fact does not conform with Dubin's hypothesis.