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Intramuscular aminotetrazole cobinamide as a treatment for inhaled hydrogen sulfide poisoning in a large swine model
Author(s) -
HendryHofer Tara B.,
Ng Patrick C.,
McGrath Alison M.,
Mukai David,
Brenner Matthew,
Mahon Sari,
Maddry Joseph K.,
Boss Gerry R.,
Bebarta Vikhyat S.
Publication year - 2020
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.14339
Subject(s) - antidote , medicine , anesthesia , intramuscular injection , respiratory system , inhalation , depression (economics) , hydrogen sulfide , toxicology , chemistry , toxicity , biology , sulfur , organic chemistry , economics , macroeconomics
Hydrogen sulfide (H 2 S), a high‐threat chemical agent, occurs naturally in a variety of settings. Despite multiple incidents of exposures and deaths, no FDA‐approved antidote exists. A rapid‐acting, easy to administer antidote is needed. We conducted a randomized control trial in swine comparing intramuscular administration of aminotetrazole cobinamide (2.9 mL, 18 mg/kg) to no treatment following inhalation of H 2 S gas. We found that aminotetrazole cobinamide administered 2 min after the onset of respiratory depression—defined as a tidal volume of less than 3 mL/kg for 2 consecutive minutes—yielded 100% survival, while all control animals died. Respiratory depression resolved in the treatment group within 3.6 ± 1.5 min (mean ± SD) of cobinamide administration, whereas control animals had intermittent gasping until death. Blood pressure and arterial oxygen saturation (SO 2 ) returned to baseline values within 5 and 10 min, respectively, of cobinamide treatment, and plasma lactate concentration decreased to less than 50% of the highest value by the end of the experiment. In control animals, plasma lactate rose continuously until death. We conclude that intramuscular aminotetrazole cobinamide is effective in a large animal, inhalational model of acute, severe H 2 S poisoning.