{'fraction_non_alphanumeric': 0.04689564068692206, 'fraction_numerical': 0.021796565389696168, 'mean_word_length': 5.108870967741935, '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}}
β-Adrenergic Receptor Subtype Effects on Stress Fever and Thermoregulation

Exposure to psychological stress increases body temperature (Tb). This stress fever may be immunologically beneficial in some patient populations but detrimental in others (e.g., HIV-infected individuals). For this reason, it is desirable to determine pharmacological methods of preventing stress fever. In rats, stress fever is modeled by exposure to a novel environment or ‘open field.’ The β-adrenergic antagonists, nadolol and propranolol, block this stress fever. Neither of these β-antagonists discriminates between subtypes of β-receptors. The purpose of this study was to determine the relative contribution of the different β-receptor types to stress fever using β1-, β2-, and β3-receptor subtype selective antagonists (atenolol [β1], ICI-118551 [β2], and SR 59230A [β3]) and agonists (dobutamine [β1], salbutamol [β2], and BRL 37344 [β3]) on the Tb of rats. Tb was measured with a biotelemetry system. Our data suggest that central nervous system β-receptor blockade with subtype-selective antagonists prevents the stress-induced rise in Tb; however, the β3-antagonist was effective only at doses that produced hypothermia in a non-stressed control group. The stress-induced fever was mimicked by central nervous system administration of the selective β2-agonist, salbutamol, and the β3-agonist, BRL 37344. We hypothesize that the blockade of stress-induced fever by β-blockers may be due to the sedative actions of these drugs.