Hemodynamic Effects of Dexmedetomidine, an α2-Adrenergic Agonist, in Autonomically Denervated Dogs

The hemodynamic effects of medetomidine continuous rate infusions in the dog

“…The increase in TPRI seen over time in all treatments exemplifies the peripheral alpha-2 receptor effect of vasoconstriction. This effect has been demonstrated in studies using autonomically denervated dogs, showing the increased vascular resistance with no change in HR (Flacke et al 1990). A previous study of medetomidine bolus dosing (Pypendop & Verstegen 1998) demonstrated an increase in systemic vascular resistance index (SVRI) with increased dose, however, in our study, only treatments 2 and 3 were significantly different from saline, and this was only at some time points.…”

Effect of dexmedetomidine vs. acepromazine–methadone premedication on limb to lung circulation time in dogs

“…The shorter CT, as well as the steeper decrease in PE'CO 2 after reaching its peak value in ACE-M group, are indicative of a reduced flow velocity in the forelimb to lung vascular segment in the DEX group. This probably applies to the whole circulation and CO (Flacke et al, 1990). Other Fig.…”

“…For this reason, their combination was chosen as the premedication for the comparison group. On the other hand, the cardiovascular side effects of dexmedetomidine are characterized by dose-dependent bradycardia, vasoconstriction and decrease in CO (Flacke et al, 1990;Lawrence, 1996). While HRs were not different between groups after induction of anaesthesia, a significant higher mean arterial pressure was observed in the DEX group.…”

“…These drugs have profound dosedependent effects on the cardiovascular system characterized by peripheral vasoconstriction, bradycardia, and decrease in CO 2 (Savola, 1989;Vainio and Palmu, 1989;Flacke et al, 1990;Bloor et al, 1992;Golden et al, 1998). Therefore, it is logical to assume that these effects will also result in prolongation of the CT which, if not taken into consideration, may lead to overdosing of anaesthetic drugs (Hall et al, 2001).…”

The use of dexmedetomidine to facilitate acute discontinuation of opioids after cardiac transplantation in children*

“…The investigators concluded that supratherapeutic doses of dexmedetomidine released intracardiac stores of catecholamines. In another study, in dogs with denervated hearts, dexmedetomidine at 1-30 g/kg produced no effect on heart rate, a 98% increase in mean arterial pressure, a 376% increase in systemic vascular resistance, and a 59% decrease in cardiac index coupled with increases in left ventricular end-diastolic pressure (15). Because the effects of dexmedetomidine were reversed with a selective ␣ 2 -antagonist and the decrease in cardiac index occurred in response to increases in systemic vascular resistance, these researchers believed that decreases in cardiac function did not result from direct effects on the myocardium.…”