We examined the mechanism of impairment of the cerebrovascular CO
2 responsiveness in moderate hypoglycemia. Twelve fasted cats were used. The brain-PO
2, brain-PCO
2 and brain-pH were measured continuously with electrodes placed on the brain surface. Hypoglycemia was induced with insulin. Intravenous injection of hexamethonium (a sympathetic ganglion blocker, C
6; 0.1mg/kg) was performed at the following stages: Control, hypoglycemia and recovery. Before and after the C
6 administration, 5%CO
2 in air was inhaled for 3 min at the respective stages. The CO
2 responsiveness (cerebrovascular dilatory response to increased P
aCO
2) at the control stage was not altered after the ganglionic blockade. At the hypoglycemic stage, the increase in BrPO
2 by CO
2 inhalation was significantly less than that at the control stage. This reduction of ΔBrPO
2 was significantly improved after the administration of C
6. At the recovery stage, the CO
2 responsiveness before and after the administration of C
6 was not significantly different. An impaired CO
2 responsiveness in the hypoglycemic state was im-proved by sympathetic ganglion blockade with C
6 which did not alter the reactivity during normoglycemia. It is suggested that the sympathetic activity plays an important role in impairment of the cerebrovascular CO
2 responsiveness during moderate hypoglycemia.
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