This experiment was performed to study pathophysiology of cerebral infarctions produced by segmental embolization of the middle cerebral artery (MCA) of the dog and the effect of embolectomy. A silicone rubber cylinder was injected into the cervical internal carotid artery and segmental occlusion of MCA was produced. Regional blood flow was measured in the ipsilateral temporal lobe by a hydrogen clearance method. Sensory evoked potential (SEP) was also recorded. Neurological deficits were evaluated after recovery from anesthesia. The site and extent of infarctions were ascertained quantitatively by an average end-area method. A separate group of dogs were subjected to embolectomy at 3 and 6 hours after embolization.
In most of the animals embolization resulted in a decrease of blood flow from the original value of 52.5±8.2 ml/100 g/min to 38.5±10.3ml/100g/min. Amplitude of SEP decreased to 70% of the resting level at 1 hour after occlusion and to 50% at 3 hours. These animals exhibited hemiplegia. Infarctions involved the lobus pyriformis, thalamus and caudate nucleus and their size reached 4.6cm3. Embolectomy at 3 hours after embolization restored cortical blood flow, accompanying reactive hyperemia. SEP increased to 110-120%. The animals were able to walk and the size of infarction was less than 1cm3. Out of 10 dogs in which embolus was removed after 6 hours, 5 could walk but other 5 could not walk or hardly walked and the mean infarct volume was 2.9cm3.
This study suggests that the perforating arteries of MCA play an important role in production of deep hemispheric infarction. Development of ischemic brain swelling seems to be the most serious risk factor for the prognosis. Measurements of r-CBF and SEP are beneficial to evaluation of the reversibiblity of brain function after ischemia.
