The alpha(2)-adrenergic agonist dexmedetomidine decreases not only hea
rt rate, myocardial. contractility, and oxygen demand, but also cardia
c output (Q). To investigate whether this reduction in Q could critica
lly impair perfusion of individual organs, we studied the effect of de
xmedetomidine on nutrient blood flow to the heart, brain, kidney, sple
en, skin, intestine, Liver, and arteriovenous anastomoses using the ra
dioactive microsphere technique. Studies were conducted in 14 dogs wit
h an open chest and anesthetized with either chloralose/urethane (CU)
or fentanyl/halothane (FH), to create different baseline conditions. H
emodynamic variables, organ blood flow, arterial and mixed venous oxyg
en, and lactate content were measured before and after administration
of 0.1, 1, and 10 mu g/kg dexmedetomidine intravenously (IV). After 10
mu g/kg dexmedetomidine Q decreased in both groups by 50%. The decrea
se in blood flow varied greatly between the organs. While now through
arteriovenous anastomoses and skin decreased by 70% to 90%, renal bloo
d flow decreased by 30%, cerebral blood flow only when baseline blood
flow was high (FH dogs), and left ventricular blood flow only in the C
U group, where the largest decrease in hemodynamic variables occurred.
Oxygen consumption decreased only in CU dogs, but so did arterial lac
tate levels. These data indicate that dexmedetomidine causes considera
ble redistribution of Q, predominantly reducing blood flow to less vit
al organs and shunt flow.