The “Low-Flow” State Following Total Cerebral Ischemia
Following 16 min of complete cerebral ischemia, produced in rats by occluding aortic outflow from the heart, cerebral perfusion rate (CPR) measured at a constant hydrostatic pressure was 7.5% of control. Epinephrine added to the perfusate increase CPR to 40.5% of control. Studies in vitro with preparations of bovine cerebral arteries disclosed two populations of these vessels: (i) arteries 0.7 to 2 mm in diameter which have no spontaneous mechanical activity and contract in a dose-related manner with potassium, epinephrine and histamine, and (ii) arteries 0.3 to 0.5 mm in diameter which have intense spontaneous activity and relax in a dose-related manner with increasing potassium concentration but which have a dose-related contraction response to epinephrine and histamine.
KeywordsCerebral Ischemia Bathing Fluid Washout Curve Cerebrovascular Resistance Aortic Outflow
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- 7.Wade, J.G., Amtorp, O., Sorensen, S.C.: Increase in the potassium concentration in brain interstitial fluid as a cause of the “no-flow” state following cerebral ischemia. In: Blood Flow and Metabolism in the Brain. Harper, A.M. (ed.). Edinburgh: Churchill Livingstone 1975, pp. 10. 26–27Google Scholar