Skip to main content
. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: Clin Toxicol (Phila). 2018 Feb 16;56(9):828–840. doi: 10.1080/15563650.2018.1429615

Figure 9.

Figure 9

(A) The left panel shows the lactate concentrations during the recovery period following the infusion of 0.75 mg/kg/min KCN for 5 min only. Blood was sampled after the end of CN exposure (time 0) then at 5, 10, 15 and 30 min. When CN infusion was stopped after 5 min, all animals survived and displayed a progressive rise in lactate reaching a maximum 10 min into recovery. The infusion of MB (20 mg/kg) or saline was started 5 min into recovery. Upon infusion of MB, lactate concentration dropped significantly (*p < .05). The administration of MB was associated (blue line) with a significantly faster recovery of O2 deficit (computed as the integral of V̇O2 over time, right panel) than when saline was infused (red line). (B) Concentrations of CN after 1 h of incubation in PBS alone (left panel) or in a solution of MB (65 μM/ml, middle panel) with an initial concentrations of CN of 200, 100, 50 and 25 μM, and in blood with an initial concentration of CN of 200 μM (right panel). CN concentrations were determined by spectrophotometry after reaction with sodium hypochlorite and barbituric acid-pyridine reagent (see method section for more details). The concentration of CN was not affected by the presence of MB in PBS but the it was lower in the blood in control condition than with MB, possibly reflecting a higher capacity of the blood to bind CN when MB was present (all tests were performed in triplicate).