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Experimental study of cerebral arterial occlusion microangiographical and histopathological findings after middle cerebral arterial occlusion

Experimental study of cerebral arterial occlusion microangiographical and histopathological findings after middle cerebral arterial occlusion

Okayama Igakkai Zasshi 98(1): 1-20

The most proximal portion of the left middle cerebral artery was occluded through the transorbital approach to produce an experimental ischemic model in dogs. It was confirmed that the middle cerebral artery was successfully occluded without any damage to the brain tissue, the anterior cerebral artery or the internal carotid artery. The 25 adult dogs used in this experiment were sacrificed between the 2nd and 21st day after the arterial occlusion, and microvascular and histopathological studies were done. The histopathological study revealed that the severity and range of infarction was variable. Infarcted areas involving the centrum semiovale and lenticular nuclei, which are mainly fed by the peripheral branches of the lenticulostriate arteries arising from proximal portion of the middle cerebral artery were found in 14 dogs. Extensive wide infarctions of the cortical and subcortical areas in addition to the peripheral territories of the lenticulostriate arteries were detected in 8 other dogs. No infarct was seen in the remaining 3 dogs. The results indicate that the peripheral area of the lenticulostriate artery is likely to be the most easily infarcted region in this experimental model. In 19 of 25 dogs, microangiography using 60% barium sulfate (Micropaque) was performed from the 2nd to the 16th day after the arterial occlusion. A remarkable midline shift to the contralateral side was a predominant finding in 2 dogs examined within 3 days of the arterial occlusion. Extravasation of contrast medium with hypervascularity in the occluded hemisphere was observed in 5 of the 8 dogs examined 4 to 7 days after the arterial occlusion. In one of the 5 dogs with these findings, extravasation was restricted in the centrum semiovale. More extensive extravasation including not only the centrum semiovale but also the internal capsule, caudate nucleus and cerebral cortex was found in 3 other dogs. In another dog, extravasated micropaque perforated via the centrum semiovale into the lateral and third ventricles. In the remaining 3 dogs examined in the same period, extravasation and hypervascularity were not so significant as in the other 5 dogs. In 7 dogs examined more than 7 days after the arterial occlusion, no notable changes in the microangiographical findings such as extravasation or hypervascularity were noted. The results indicate that extravasation and hypervascularity are observed 4 to 7 days after the arterial occlusion in this experimental model, which suggests that vascular vulnerability might be increased to the greatest extent in this period. If true, this hypothesis may give one reason why spontaneous recanalization or surgical reconstruction of occluded vessels in this subacute period not infrequently causes hemorrhagic infarction, followed by further deterioration of symptoms and signs.

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