Sympathetic activity enhances glucose-related ischemic injury in the rat

Studies have shown that increased sympathetic activity or increased blood and brain glucose concentration worsen postischemic brain damage. The authors evaluated the interaction of plasma glucose with epinephrine and norepinephrine during incomplete cerebral ischemia in the rat using ganglionic blockade.

Rats were anesthetized with 25 micrograms.kg-1.h-1 fentanyl and 70% nitrous oxide in oxygen. Ganglionic blockade was produced in 30 rats using 8 mg/kg hexamethonium intravenously. Three plasma glucose ranges, low < 150 mg/dl, moderate = 150-300 mg/dl, and high > 300 mg/dl, were produced in each group. Ischemia was induced by unilateral carotid ligation and hemorrhagic hypotension to 30 mmHg for 30 min. Plasma norepinephrine and epinephrine were measured by radioimmunoassay. Neurologic outcome was evaluated daily for 3 days after ischemia.

Ganglionic blockade decreased blood pressure before the start of ischemia and plasma epinephrine and norepinephrine during ischemia (P < 0.05). Neurologic outcome was significantly worse in rats with high glucose compared with low glucose concentrations with and without ganglionic blockade (P < 0.05). Neurologic outcome and stroke-related mortality were worse in rats with increased plasma epinephrine and norepinephrine compared with rats with ganglionic blockade when plasma glucose was less than 300 mg/dl (P < 0.05).

These results indicate that increased concentration of catecholamines enhance glucose-related injury during incomplete ischemia in rats.