Restoration of Middle Cerebral Artery Flow in Experimental Infarction

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At the present time a patient with an acute middle cerebral artery occlusion represents an unanswered challenge for effective treatment. Conservative management has done little to alter the size of the resulting cerebral infarctions and the magnitude of related neurological deficits. Although occasional young persons withstand this catastrophe,1 these patients generally do poorly, and the survivors can hardly be called therapeutic successes.6

The purpose of this work was to determine what benefits and hazards might be anticipated if flow through an occluded middle cerebral artery could be restored. Possible protective measures of hemodilution were investigated,

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New address: Section of Neurosurgery, Mayo Clinic, Rochester, Minnesota 55901.

© AANS, except where prohibited by US copyright law.

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    Monkey parietal cortex prior to occlusion of middle cerebral artery. Slight pallor from light reflex is artifact.

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    Cerebral cortex 30 minutes following MCA occlusion. Pallor is developing in cortex; veins become darker (poorly shown in this slide).

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    Cerebral cortex 1 hour following occlusion. Pallor is progressing; venous sludging present.

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    Cerebral cortex 3 hours following occlusion. Arterial spasm present in areas of pallor; venous sludging more marked.

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    Cerebral cortex 5 minutes following removal of occluding slip. Cortex is recolorizing, spasm reversing.

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    Cerebral cortex 30 minutes following removal of occluding clip. Veins are redder; entire cortex has background hyperemia. (Luxury perfusion syndrome of Lassen.)

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    Infarction followed permanent MCA occlusion, no treatment: The animal died 24 hours after surgery, after having awakened from anesthesia. The degree of edema was typical of this group of animals.

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    Infarction following permanent MCA occlusion with hemodilution. Following occlusion of the vessel the animal was treated by hemodilution with albumin and low molecular weight dextran. The degree of edema was typical in this group of animals. The animal died 16 hours after surgery, after having awakened from anesthesia.

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    Infarction following 6 hours of MCA occlusion, no treatment. Small areas of hemorrhage in this specimen were uncommon in the group as a whole. The large amount of edema was typical of the group. This animal died 20 hours after surgery, after having awakened from anesthesia.

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    Infarction following 6 hours of MCA occlusion with hemodilution. During period of occlusion the animal was treated with hemodilution using albumin and low molecular weight dextran. The degree of edema shown is typical for this group. The animal died 3 days following surgery and had a severe hemiplegia before death.

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    No infarction 3 hours after MCA occlusion, with no hemodilution. The animal was killed 1 week after surgery; he had no paresis at the time of death.

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    No infarction 3 hours after MCA occlusion; hemodilution with albumin alone. The animal had no paresis at the time of death and was killed 1 week after surgery.

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    Infarction following 3 hours of MCA occlusion and hemodilution with albumin and low molecular weight dextran. This degree of edema was typical for this group. The animal died 16 hours after surgery.

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    The brain on the left shows a typical cerebral infarction in a cat with permanent middle cerebral artery occlusion. The brain on the right shows a typical absence of infarction following 6 hours of occlusion of this vessel.

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    Left: Preoperative arteriogram on a patient with an acute middle cerebral artery occlusion. Later films in the arterial sequence demonstrated collateral filling of the region of the middle cerebral artery. Right: Postoperative arteriogram in same patient. The time interval between vessel occlusion and operative opening was 12 hours. The patient was improved postoperatively.

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