{'fraction_non_alphanumeric': 0.02702702702702703, 'fraction_numerical': 0.017436791630340016, 'mean_word_length': 5.792899408284024, '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}}
Lipoxygenase inhibitors block O2 responses of hamster cheek pouch arterioles.

The hypothesis that a lipoxygenase is involved in arteriolar oxygen reactivity was tested in the superfused hamster cheek pouch preparation by assessment of the effects of three lipoxygenase inhibitors on the response of arterioles to changes in superfusate PO2. Superfusion of hamster cheek pouches with nordihydroguaiaretic acid (NDGA), 5,8,11,14-eicosatetraynoic acid (20 microM ETYA), or 100 microM 1-phenyl-3-pyrazolidone (phenidone) decreased (10 microM NDGA) or eliminated (30 microM NDGA, ETYA, or phenidone) the constriction of arterioles induced by elevation of superfusate oxygen tension. The response of the arterioles to the alpha 1-adrenergic agonist phenylephrine was not significantly affected by these inhibitors, an indication that the decreased oxygen response was not due to a nonspecific decrease in arteriolar reactivity. These data suggest that arteriolar oxygen reactivity in the hamster cheek pouch might involve a lipoxygenase or other noncyclooxygenase oxygen-dependent biochemical pathway that can be inhibited by NDGA, ETYA, and phenidone.