Uncoupling of blood flow and glucose metabolism in the neighboring postischemic edematous brain area.

Postischemic events cause exacerbation of brain injury, not only in the postischemic area but also in the area originally free from the ischemic insult. The present study was performed in rats. After the animals were anesthetized with a mixture of 70% N2O, 0.5% halothane, a focal ischemia was induced by occlusion of the right MCA by means of a silicone rubber cylinder introduced from the internal carotid artery. Three hours after the MCA occlusion, the embolus was pulling out from the artery by an attached nylon surgical thread. Three hours after the recanalization, animals were decapitated to acquire water content of the brain, local CBF, or local CMRgl. After recirculation, water content markedly increased in the MCA area whereas the CBF returned near normal. However, the CMRgl decreased below half of the normal value. In the neighboring, originally nonischemic area, water content remained within the normal limit although the CBF markedly decreased and the CMRgl increased. Deductions from these data were as follows: (a) If the brain tissue cannot recover from the ischemic-induced injury, restored blood flow may exacerbate the brain edema; and (b) the edematous brain tissue affects the neighboring area with lowering blood flow and rising glucose consumption.