{'fraction_non_alphanumeric': 0.023875114784205693, 'fraction_numerical': 0.01652892561983471, 'mean_word_length': 5.411764705882353, '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}}
Defect of urinary concentration capacity in cephaloridine-administered rats.

The nephrotoxic effects of cephaloridine on the renal concentration capacity were examined in rats that had received a single intravenous injection of cephaloridine (100 or 500 mg/kg body weight). An increase in urinary volume and a decrease in urinary osmotic pressure were observed continuously from the first to the sixth day in the 500 mg/kg group, but not in the 100 mg/kg group. In addition, rises in plasma levels of arginine-vasopressin were observed in the 100 and 500 mg/kg groups. Furthermore, responsiveness to exogenous arginine-vasopressin was investigated in the cephaloridine-administered rats under ethanol anesthesia. The injection of arginine-vasopressin caused relatively slight responses, in terms of the urine flow and urinary osmolality, in the cephaloridine-administered group in comparison to the control group. these findings indicate that cephaloridine induces a vasopressin-resistant polyuria, and strongly suggest that cephaloridine does damage the collecting tubules in the kidney.