BRAIN ALPHA-2-ADRENERGIC RECEPTOR-BINDING DURING INCOMPLETE CEREBRAL-ISCHEMIA IN THE RAT

Alpha2-adrenergic agonists decrease sympathetic activity and improve outcome from brain ischemia. We evaluated whether changes in alpha2-adrenergic receptor binding activity may be important in the sympathetic depressant and cerebral protective effects of halothane (1.1 % inspired) or isoflurane (1.4% inspired) compared to fentanyl/nitrous oxide (N2O) anesthesia. Brain alpha2-adrenergic receptor binding was measured using [H-3]-clonidine in each of four treatment conditions: 1, unanesthetized; 2, anesthetized (fentanyl/N2O, halothane, or isoflurane): 3, anesthetized with ischemia; 4, after 4 h recovery from ischemia. Ischemia was produced by right carotid artery ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Both halothane and isoflurane decreased alpha2-adrenergic receptor density 20% compared to unanesthetized values (P < 0.01). This decrease was attenuated in ischemic tissue. There were no consistent changes in receptor affinity. These results suggest that inhaled anesthetics decrease the number of alpha2-adrenergic receptors. This decrease appears to be unrelated to plasma catecholamine concentrations but may be influenced by the degree of ischemia.