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(Stroke. 1995;26:1107-1113.)
© 1995 American Heart Association, Inc.

Articles

Chronic Depression of Glucose Metabolism in Postischemic Rat Brains

Thomas Beck, PhD; Hans-Joachim Goller, MD Andreas Wree, MD

From the Institut für Anatomie der Universität Rostock (Germany).

Correspondence to Thomas Beck, PhD, Institut für Anatomie der Universität Rostock, Gertrudenstr 9, PO Box 10-08-88, D-18055 Rostock, Germany. E-mail beck@medizin.uni-rostock.d400.de.

Background and Purpose The present investigation aimed to quantify functional activity in rat brains after long-term recovery from transient forebrain ischemia.

Methods With the use of the [¹⁴C]2-deoxyglucose method, local cerebral glucose utilization was measured in 62 cortical and subcortical brain regions in postischemic rat brains. Transient forebrain ischemia of 10 minutes' duration was induced by clamping the common carotid arteries and simultaneously lowering blood pressure to 40 mm Hg. Rats survived the insults for 1 week, 2 weeks, 3 weeks, or 3 months.

Results Reductions predominated in the majority of gray matter structures at all time points investigated (P<.05). Except for a few areas, recoveries of local cerebral glucose utilization to preischemic levels did not occur.

Conclusions The data illustrate that widespread alterations of functional activity prevail in postischemic brains beyond the selectively vulnerable regions. The present functional data are in line with previous stereological results of reduced fresh volumes in the majority of postischemic brain structures. The data suggest that chronic alterations of ischemic brains are not confined to the selectively vulnerable regions.

Key Words: cerebral ischemia • glucose • rats