The interaction of plasma
catecholamines and
nitrous oxide (N2O) ventilation was examined during
brain ischemia in rats. Group 1 (n = 19) was anesthetized with 50 micrograms.kg-1 x h-1 of
fentanyl and ventilated with 70%
nitrogen in
oxygen. Group 2 (n = 19) was anesthetized with intravenous
fentanyl (25 micrograms.kg-1 x h-1) and 70% N2O ventilation in
oxygen. Group 3 (n = 10) received 25 micrograms.kg-1 x h-1 of
fentanyl and 70% N2O ventilation and 100 micrograms/kg of
dexmedetomidine, an alpha 2-adrenergic receptor agonist that decreases sympathetic activity. Incomplete
brain ischemia was produced by right carotid
ligation combined with hemorrhagic
hypotension to 30 mm Hg for 30 min. Plasma
catecholamines were measured during
ischemia. Cerebral blood flow (CBF) was evaluated by using
laser Doppler. Neurologic outcome was evaluated for 3 days after
ischemia. Plasma
epinephrine and
norepinephrine and were decreased 20% and neurologic outcome was significantly worse in Group 2 ventilated with N2O compared with
fentanyl-anesthetized controls (P < 0.05).
Dexmedetomidine-treated rats had lower plasma
catecholamines (20% of control) and larger decreases in CBF during
ischemia compared with controls.
Dexmedetomidine (Group 3) improved outcome from
ischemia in comparison to both Groups 1 and 2 (P < 0.05). These results suggest that
catecholamines play a major role in worsening ischemic outcome. N2O ventilation may increase neuronal injury by enhancing the sympathetic response to
ischemia.