{'fraction_non_alphanumeric': 0.013802622498274672, 'fraction_numerical': 0.004830917874396135, 'mean_word_length': 5.387665198237886, '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}}
The secondary and tertiary inflammatory cellular reaction in arterioles damaged by acute angiotensin-hypertension in rats.

When rats were treated repeatedly with series of intravenous injections of angiotensin, intervals between the series covering at least one week, the cellular reaction in the arterioles damaged by the hypertension differed from that to be found after only one series of injections (primary reaction). While the primary reaction showed equal numbers of mononuclear cells and polymorphous leucocytes at onset of the luminal cellular reaction and a duration of about 72 hours, the secondary and tertiary reactions differed (in identical way) with dominance of mononuclear cells from onset and to termination of the cellular reaction, with appearance of polymorphous leucocytes in the adventitia, and with a markedly prolonged duration of the reaction, up to more than 96 hours. Finally, the total number of mononuclear cells which infiltrated the damaged arterioles after the termination of the second and third hypertensive period was 3–10 times higher than that found after the first hypertensive period. It was found that the changed reaction was not caused by a development of impaired areas of the arterioles damaged during the first hypertensive period. As the secondary reaction has much in common with a delayed type of hypersensitivity the possible antigen was discussed, and angiotensin was found not to be responsible.