1 Department of Neurosurgery, Massachusetts General Hospital, Boston, Massachusetts; National Institute of Neurological Diseases and Stroke, U. S. Public Health Service; Current address: Department of Neurosurgery, Children's Hospital Medical Center, 300 Longwood Avenue, Boston, Massachusetts
Reperfusion of cerebral vessels is impaired following total cerebral ischemia of more than five minutes; this is possibly the initial factor responsible for neurological sequela. Failure of cellular ion transport mechanisms during ischemia was thought to lead to swelling of endothelial cells and perivascular glia and this, in turn, was thought to be the primary cause of the impairment of recirculation. A method of quantitating this circulatory impairment in rabbits was devised after infusing carbon black into the ischemic cerebral vasculature in a standardized way. The amount of circulatory impairment was shown to be unaffected by heparin, inversely related to the infusion pressure of the carbon black, and greatly reduced by acute hemodilution with saline. This latter observation does not support the theory that cellular swelling is the major cause of the postischemic vascular impairment, but rather implicates changes in the blood itself, possibly erythrocyte aggregation which is responsible for increased blood viscosity in low flow and no flow states.
© 1972 American Heart Association, Inc.
Studies on Mechanisms of Impairment of Cerebral Circulation Following Ischemia: Effect of Hemodilution and Perfusion Pressure
2 Department of Neurosurgery, Massachusetts General Hospital, Boston, Massachusetts; National Institute of Mental Health, U. S. Public Health Service
Key Words: cerebral ischemia • circulatory impairment • erythrocyte aggregation
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