Abstract
Collapse of the microcirculation is always among the factors contributing to the evolution of ischemic tissue damage in the brain. The approach to assess the progress of failure in the ischemic parenchymal circulation taken by the present study was to monitor the erythrocyte and plasma microflows along with local tissue hematocrit in a two dimensional plane at high topographical and temporal resolution by a television densitometric method3,4 in the intact cerebrocortical tissue. Preliminary studies with this method have revealed significant heterogeneity of these parameters under control conditions. It was postulated that the decisively different microhemodynamic behavior of erythrocytes and plasma could focally be further accentuated under ischemic conditions (endothelial lesions, vasoaction, edema, obstruction and occlusion of the capillary network) and may lead to a dissociation of erythrocyte and plasma channels manifested by marked focal alterations in tissue hematocrit and an altered distribution pattern of microflows. To test this hypothesis, global cerebral ischemia was induced and maintained by adjusting the mean arterial blood pressure to 40 mmHg by controlled arterial hemorrhage.
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© 1989 Plenum Press, New York
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Eke, A. (1989). Hematocrit Changes in the Extra- and Intraparenchymal Circulation of the Feline Brain Cortex in the Course of Global Cerebral Ischemia. In: Rakusan, K., Biro, G.P., Goldstick, T.K., Turek, Z. (eds) Oxygen Transport to Tissue XI. Advances in Experimental Medicine and Biology, vol 248. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5643-1_49
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DOI: https://doi.org/10.1007/978-1-4684-5643-1_49
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