• Y Kalam and A Graudins.
• Southern Health Emergency Medicine and Toxicology Research Group, Southern Clinical School, Monash University, Clayton, Victoria.
• Hum Exp Toxicol. 2012 Sep 1;31(9):955-63.

UnlabelledLevosimendan (Levo) is an inodilator improving cardiac output (CO) and reducing afterload in heart failure. Previously, we reported that Levo improved CO but not blood pressure (BP) in a rodent model of verapamil poisoning. We theorised that Levo-induced vasodilation should not influence BP to a similar degree in metoprolol poisoning.AimTo assess the effect of Levo on haemodynamics in a rodent model of metoprolol poisoning.MethodAnaesthetized male Wistar rats were infused metoprolol continuously. When the BP dropped to 50% of baseline (time 0) rats received 1 of the 4 treatments: (a) control (0.9% saline bolus + infusion); (b) Levo-l (Levo 36 μm/kg loading dose followed by 0.6 μm/kg/min); (c) Levo-I (Levo infusion only at 0.6 μm/kg/min); and (d) Epi (epinephrine 0.5 μm/kg/min). All groups received comparable fluid volumes. Haemodynamics were recorded every 10 min for 70 min. CO, mean arterial pressure (MAP) and heart rate (HR) of each group were compared to the control.ResultsAll groups had comparable baseline and time 0 HR, MAP and CO. Levo-L and Levo-I rats showed significantly greater CO at t = 10 min (p > 0.02 and p > 0.04, respectively). CO was higher at all other time points for both Levo groups. This was not statistically significant. Levo did not improve MAP compared to control. Adrenaline increased MAP but not CO compared to control and Levo groups.ConclusionLevo did not improve MAP but moderately improved CO compared to control in this model of metoprolol poisoning. The response was similar to that reported previously in verapamil-poisoned rats. The improvement in MAP seen with epinephrine was most likely vasoconstriction mediated.

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