Academic emergency medicine : official journal of the Society for Academic Emergency Medicine · 2003
Sodium thiosulfate fails to reduce nitrite-induced methemoglobinemia in vitro.
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Matteucci Michael John, Reed William Job, Tanen David Alan
Аннотация
OBJECTIVES: To determine whether sodium thiosulfate (STS) produces a clinically significant decline in sodium nitrite-induced methemoglobinemia in an in-vitro model.
METHODS: This was an in-vitro, controlled study where methemoglobinemia was induced by the addition of sodium nitrite (0.4 mg/mL) to 35-mL aliquots of blood obtained from ten healthy volunteers. Methemoglobin (MetHb) concentrations were measured at 5-minute intervals for 30 minutes by co-oximetry, and each aliquot was then subdivided into six 5-mL samples (time zero). Sample 1 served as control. The remaining samples received serial dilutions of STS (0.125 mg, 1.25 mg, 12.5 mg, 125 mg, 1,250 mg). MetHb concentrations were measured by co-oximetry at baseline, 0, 15, 30, 45, and 60 minutes. Areas under the MetHb concentration-time curve (AUC) between time zero and 60 minutes were compared using the Kruskal-Wallis test.
RESULTS: Methemoglobin concentrations increased from 0.07 g/dL (+/-0.06) at baseline to 8.42 g/dL (+/-0.69) at time 0 (the addition of STS). No significant difference was detected between baseline and time 0 hemoglobin concentrations (15.8 +/- 0.5 vs. 16.1 +/- 0.6 g/dL). There was no detectable difference found between the AUCs (measured in g min/dL) of any of the STS serial dilutions or control groups (0.125 mg STS = 576.01 +/- 42.53; 1.25 mg STS = 573.47 +/- 40.82; 12.5 mg STS = 583.68 +/- 42.29; 125 mg STS = 554.75 +/- 42.68; 1,250 mg STS = 566.95 +/- 38.08; p = 0.81).
CONCLUSIONS: Sodium thiosulfate was not found to be an effective reducing agent for the acute treatment of methemoglobinemia.
METHODS: This was an in-vitro, controlled study where methemoglobinemia was induced by the addition of sodium nitrite (0.4 mg/mL) to 35-mL aliquots of blood obtained from ten healthy volunteers. Methemoglobin (MetHb) concentrations were measured at 5-minute intervals for 30 minutes by co-oximetry, and each aliquot was then subdivided into six 5-mL samples (time zero). Sample 1 served as control. The remaining samples received serial dilutions of STS (0.125 mg, 1.25 mg, 12.5 mg, 125 mg, 1,250 mg). MetHb concentrations were measured by co-oximetry at baseline, 0, 15, 30, 45, and 60 minutes. Areas under the MetHb concentration-time curve (AUC) between time zero and 60 minutes were compared using the Kruskal-Wallis test.
RESULTS: Methemoglobin concentrations increased from 0.07 g/dL (+/-0.06) at baseline to 8.42 g/dL (+/-0.69) at time 0 (the addition of STS). No significant difference was detected between baseline and time 0 hemoglobin concentrations (15.8 +/- 0.5 vs. 16.1 +/- 0.6 g/dL). There was no detectable difference found between the AUCs (measured in g min/dL) of any of the STS serial dilutions or control groups (0.125 mg STS = 576.01 +/- 42.53; 1.25 mg STS = 573.47 +/- 40.82; 12.5 mg STS = 583.68 +/- 42.29; 125 mg STS = 554.75 +/- 42.68; 1,250 mg STS = 566.95 +/- 38.08; p = 0.81).
CONCLUSIONS: Sodium thiosulfate was not found to be an effective reducing agent for the acute treatment of methemoglobinemia.