Hyperglycemia has been reported to worsen the tolerance of the brain to ischemia, and it has therefore been recommended that patients undergoing neurosurgical procedures not receive glucose-containing solutions. However, whereas most animal studies have used global ischemia models, most neurosurgical procedures are associated with risks of focal rather than global ischemia. We therefore studied the effects of glucose administration in an animal model of focal cerebral ischemia. We anesthetized 20 cats with halothane (0.85% end tidal in oxygen), and a focal cerebral ischemic lesion was produced by clip ligation of the left middle cerebral artery using a transorbital approach. Hyperglycemia (10 cats, mean±SEM plasma glucose concentration 561 ±36 mg/dl) was established before ligation by infusion of 50% glucose in 0.45% saline; the control group (10 cats, mean±SEM plasma glucose concentration 209±28 mg/dl) received 0.45% saline only. Total fluid administered, mean arterial blood pressure, body temperature, and arterial blood gas values did not differ between the two groups 0, 2, and 6 hours after ligation. The cats were killed 6 hours after ligation, and the area of severe ischemic neuronal damage was determined by microscopic examination of a coronal section at the level of the optic chiasm. The mean±SEM area of left cortical severe ischemic neuronal damage was 12±2% of the left cortex in the hyperglycemic group compared with 28±5% in the control group (/><0.01). The area of severe ischemic neurologic damage was inversely related to plasma glucose concentration, for both all cats (r=0.69) and for the control cats alone (r=0.80). We conclude that glucose may protect the brain from severe, focal, ischemic neuronal damage and that further studies are needed to document the efficacy and mechanisms of protection. (Stroke 1989;20:519-523) I n models of global cerebral ischemia, hyperglycemia increases both morphologic brain damage 1 -3 and the severity of neurologic deficits. 4 -3 In these models, temporary global cerebral ischemia is produced by a variety of techniques (including hypoxia, hemorrhage, tourniquet interruption of cerebral blood flow, surgical occlusion of the cerebral vessels, induced hypotension, and cardiac arrest), often in combination, followed by restoration of normal cerebral oxygenation and cir- Received July 13, 1988; accepted September 8, 1988. culation. However, the generalizability of these models to clinical practice is debatable since cerebral ischemia in humans is often focal rather than global. Interventions may have different effects in focal compared with global cerebral ischemia. For example, the administration of barbiturates before ischemia appears to provide protection from focal cerebral ischemia 67 but is ineffective in global ischemia. 8 The effect of hyperglycemia on focal cerebral ischemia remains controversial. Several studies suggest that hyperglycemia worsens the injury, 9 -" whereas others suggest that it either decreases 1213 or has no effect on 14 the extent of cerebral ...
