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Stroke

Microcirculatory obstruction in focal cerebral ischemia: albumin and erythrocyte transit.

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J R Little
A Cook
S A Cook
W J MacIntyre

Mots clés

Abstrait

The objectives were to study plasma and erythrocyte flow in an area of acute focal cerebral ischemia and define their relationship to developing microcirculatory obstruction as determined by morphological techniques. Eighteen adult cats, anesthetized with ketamine hydrochloride, had right middle cerebral artery (MCA) occlusion. Plasma flow was determined by measuring the transit of Iodine-131 (131I) albumin and erythrocyte flow was determined by measuring the transit of Technetium-99 (99Tc) labeled erythrocytes in the right Sylvian region. Transit studies were performed before and immediately after right MCA occlusion and at the end of the ischemic period, 1 hour, 3 hours, or 6 hours after occlusion. Intra-arterial perfusion with a buffered formaldehyde - colloidal carbon solution was carried out after completion of the isotope studies. Swelling of cerebral tissue and impaired carbon filling in the right MCA territory were seen initially after 3 hours occlusion and were more severe after 6 hours occlusion. Ischemic neuronal alterations, edema formation, and capillary luminal narrowing increased with longer periods of occlusion. 131I albumin transit time in the right Sylvian region was 8 +/- 2 seconds before occlusion and 10 +/- 2 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. Transit times increased progressively with longer periods of occlusion in cats developing cortical ischemic changes. No evidence of complete microcirculatory obstruction to albumin and erythrocyte transit was seen in cats with 6 hours of occlusion despite the impaired filling of the cortical microcirculation with carbon. There were no findings to substantiate the hypothesis that plasmapheresis develops during the early phases of cerebral infarction.

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