Abstract
Regional cerebral ischemia was induced in dogs by injecting a silicone rubber cylinder through the cervical internal carotid artery. The embolus was found to be lodged in the proximal portion of the middle cerebral artery in 33 dogs, distal portion of the middle cerebral artery in seven dogs, anterior cerebral artery in 11 dogs, posterior communicating artery in three dogs and osseous portion of the internal carotid artery in five dogs. Cerebral ATP and lactate and protein concentrations were quantitatively analysed in the parietal lobe, temporal lobe and basal ganglia of both the embolized and non-embolized hemispheres of each group. Relationships between the neurological signs and the changes in regional brain energy metabolism of each group were studied. In the group in which the embolus was lodged in the proximal portion of the middle cerebral artery, ATP depletion and lactate accumulation were most predominant in the basal ganglia of the embolized hemisphere. Disturbed consciousness and hemiparesis were observed. In the group in which the embolus was lodged in the distal portion of the middle cerebral artery, ATP depletion was evident only in the temporal lobe of the embolized hemisphere. Hemianopsia was observed in two of the three animals. In the group in which the embolus was lodged in the anterior cerebral artery, no neurological defect could be observed except in one animal showing disturbed consciousness and hemiparesis. This animal showed ATP depletion in the basal ganglia of the embolized hemisphere probably caused by obstruction of the perforating arterial branches from the anterior cerebral artery. In the group in which the embolus was lodged in the posterior communicating artery, protein concentration was decreased remarkably at all sites in the embolized hemisphere. It was considered to be acute brain swelling. Animals were comatose, and one of them died 3 hours after embolization. It was suggested that hypothalamus or posterior thalamus, the territory of the posterior communicating artery, might play an important role in causing acute brain swelling. In the group in which embolus was lodged in the osseous portion of the internal carotid artery, no neurological defect nor any change in energy metabolism could be seen. Regional energy metabolism was analysed 1, 3, 5, 12, 24 hours after embolization of the proximal middle cerebral artery. ATP levels in the basal ganglia of the embolized hemisphere which is the ischemic focus of this group decreased linearly up to 5 hours after embolization but were restored to the resting level 12 hours after embolization and were depleted again 24 hours after embolization. The transient restoration of the ATP values probably occurred because ischemic cell damage first took place at the site of ATP consumption such as a synapse rather than at the mitochondria where ATP was synthesized.
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