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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.
Hoffman et al. (Mon,) studied this question.