Methadone Increases and Prolongs Detomidine-Induced Arterial Hypertension in Horses, but These Effects Are Not Mediated by Increased Plasma Concentrations of Arginine Vasopressin or Serum Concentrations of Catecholamines

• The aim of the study was to determine if cardiovascular activation by methadone (MET) is mediated by arginine vasopressin (AVP).
• Six mature horses sedated IV with detomidine alone or with MET were used.
• Detomidine induces a short-term mean arterial blood pressure increase.
• This effect was prolonged and potentiated by MET association.
• There are no evidences of AVP, noradrenaline, and adrenaline involvement in this effect.

Catecholamines and arginine vasopressin (AVP) release can affect arterial blood pressure (ABP) and hemodynamic stability in standing, sedated horses. Six mature horses were included in this prospective, randomized, crossover, blinded, experimental study. All the horses were sedated with detomidine (DET) alone (0.01 mg/kg, IV) or combined with methadone (MET) (0.01 mg/kg DET and 0.2 mg/kg MET, IV). Cardiopulmonary data and blood samples were collected 30 minutes before (prebaseline and baseline) and for 120 minutes postinjection. The combination DET/MET produced a significant increase (31%) in mean ABP (MAP) 5 minutes after drug administration which lasted for 120 minutes. Detomidine alone induced only a short-term increase in MAP (15%) at 5 minutes compared with baseline. There were significant differences between groups at 5, 15, and from 60 to 120 minutes. Plasma AVP concentrations were higher in horses receiving the treatment DET from 60 to 120 minutes than those in the combination group, for the same period. There were no significant differences in norepinephrine and epinephrine serum concentrations respect to baseline and between treatments. Detomidine induces a short-term MAP increase, and this effect was prolonged and potentiated by MET association. There is no evidence of AVP, norepinephrine, and epinephrine involvement in this effect.