{'fraction_non_alphanumeric': 0.045701357466063346, 'fraction_numerical': 0.04253393665158371, 'mean_word_length': 5.090909090909091, '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}}
Resuscitative effect of a gamma-aminobutyric acid B receptor antagonist on gamma-hydroxybutyric acid mortality in mice.

STUDY OBJECTIVE
In the present study, a number of compounds were tested to evaluate their efficacy in exerting a protective effect on gamma-hydroxybutyric acid (GHB)-induced mortality in mice. The drugs investigated were the gamma-aminobutyric acid B (GABA B ) receptor antagonist SCH 50911, the GABA A receptor antagonist bicuculline, the benzodiazepine receptor antagonist flumazenil, the putative GHB receptor antagonist NCS-382, the opioid receptor antagonist naltrexone, and the amino acid and possible neuromodulator, taurine.


METHODS
All mice were initially treated with a lethal dose of GHB (7 g/kg, administered intragastrically). Once mice had displayed clear signs of GHB intoxication, animals from each group were treated acutely with either SCH 50911 (vehicle; 75, 150, and 300 mg/kg, administered intraperitoneally), bicuculline (vehicle; 2, 4, 6, and 8 mg/kg, administered intraperitoneally), flumazenil (vehicle; 1, 3, and 10 mg/kg, administered intraperitoneally), NCS-382 (vehicle; 50 and 200 mg/kg, administered intraperitoneally), naltrexone (vehicle; 3 and 10 mg/kg, administered intraperitoneally), or taurine (vehicle; 250 and 750 mg/kg, administered intraperitoneally). The various doses of each single drug were administered to 10 mice, randomly allocated throughout the experimental groups. Mortality was recorded every hour for the first 9 hours and subsequently 12, 18, and 24 hours after GHB injection.


RESULTS
In each experiment, all vehicle-treated mice died within 24 hours of GHB injection. Doses of 150 and 300 mg/kg SCH 50911 produced a marked protection on GHB-induced mortality, evidenced by the death of only 0 of 10 and 2 of 10 mice in the 150- and 300-mg/kg SCH 50911 groups, respectively. In contrast, at all doses tested, bicuculline, flumazenil, NCS-382, naltrexone, and taurine were not observed to exert any protective effect on GHB-induced mortality (9 to 10/10 mice died in each treatment group).


CONCLUSION
These results suggest an involvement of the GABA B receptor, at least in rodents, in the mediation of the lethal effects of GHB.