EFFECT OF OXYGEN AND SODIUM THIOSULFATE DURING COMBINED CARBON-MONOXIDE AND CYANIDE POISONING

In a canine model of combined carbon monoxide (CO) and cyanide (CN) po isoning, cardiac output (Q(T)) and oxygen consumption (V-o2) decreased but recovered to baseline values by 15 min after toxic exposure; elev ated blood CN and lactic acidosis persisted for at least another 10 mi n. Given the rapid spontaneous recovery after cessation of toxic expos ure, we questioned the efficacy of usual treatment with oxygen (O-2) a nd sodium thiosulfate (Na2S2O3) for CN poisoning. Accordingly, in seve n dogs (26 +/- 3 kg, chloralose and urethane anesthesia), we sequentia lly administered CO by closed circuit inhalation (231 +/- 42 ml) and p otassium CN by intravenous infusion (0.072 mg . kg(-1). min(-1) for 17 +/- 3 min). Fifteen minutes after toxic exposure, 02 breathing began and Na2S2O3 (150 mg/kg) was infused. Measurements were repeated 10 and 45 min after treatment. At the end of the CN infusion, Q(T) decreased by 43% and V-o2 decreased by 51%, compared to baseline values. Both v ariables recovered to baseline by 15 min after stopping toxic exposure . Significant lactic(4.8 +/- 2.9 mM) acidosis (7.14 +/- 0.10) persiste d for at least another 10 min. Treatment with oxygen and Na2S2O3 did n ot hasten the recovery of this lactic acidosis or decrease blood cyani de levels compared to nontreated dogs, However, after treatment, plasm a thiocyanate significantly increased from 16.3 +/- 12.5 to 94.4 +/- 7 2.2 mu M, as Na2S2O3 participated in the increased metabolism of cyani de to thiocyanate. We conclude that O-2 and Na2S2O3 therapy should be continued during combined CO and HCN poisoning. Oxygen increases CO el imination and can enhance anti-CN treatment. After infusion or inhalat ion of CN, when most CN has already penetrated the intracellular compa rtment, postexposure sodium thiosulfate increased the metabolism of CN . (C) 1995 Academic Press, Inc.