{'fraction_non_alphanumeric': 0.029097963142580018, 'fraction_numerical': 0.016488845780795344, 'mean_word_length': 4.931034482758621, '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 role of hypoxia in the hyperglycaemic effect of xylazine in sheep.

Xylazine (0.2 mg/kg, i.v.) was administered to sheep breathing room air (group X) or oxygen (group XO). Xylazine induced a rise in serum glucose concentration which, following a sharp increase in the first 30 minutes, remained at similar high levels (about 165% of the pre-injection value) for another 2.5 hours. Arterial PCO2 was slightly increased and reached a significant level at 5 and 15 minutes following xylazine injection in group X. In group XO, at all sampling times after the injection, PaCO2 showed a similar pattern of increase, although the effect was not significant. Arterial PO2 was decreased significantly for at least 60 minutes. Hypoxia by itself can induce hyperglycaemia, but its prevention by administering oxygen did not alter the hyperglycaemic effect of xylazine. It was concluded that the hypoxia following administration of xylazine was not severe enough to produce a rise in catecholamine concentrations eliciting hyperglycaemia.