The “Low-Flow” State Following Total Cerebral Ischemia

  • J. G. Wade
  • W. A. Tweed
  • W. J. Davidson
Conference paper


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.


Cerebral Ischemia Bathing Fluid Washout Curve Cerebrovascular Resistance Aortic Outflow 
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  1. 1.
    Edvinsson, L., Aubineau, P., Owman, C., Sercombe, R., Seylaz, J.: Sympathetic innervation of cerebral arteries: prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment. Stroke 6, 525–530 (1975)PubMedCrossRefGoogle Scholar
  2. 2.
    Eidelman, B.H., McCalden, T.A., Rosendorf, C.: The role of the carotid body in mediating the cerebrovascular response to altered arterial carbon dioxide tension. Stroke 7, 72–76 (1976)PubMedCrossRefGoogle Scholar
  3. 3.
    James, I.M., Miller, R.A., Purves, M.J.: Observations on the extrinsic neural control of cerebral blood flow in the baboon. Circulat. Res. 25, 77–93 (1969)PubMedGoogle Scholar
  4. 4.
    Krnjevic, K., Morris, M.E.: Extracellular accumulation of K+ evoked by activity of primary afferent fibers in the cuneate nucleus and dorsal horn of cats. Canad. J. Physiol. 52, 852–871 (1974)CrossRefGoogle Scholar
  5. 5.
    Lassen, N.A.: Control of cerebral circulation in health and disease. Circulat. Res. 34, 749–760 (1974)PubMedGoogle Scholar
  6. 6.
    Wade, J.G., Amtorp, O., Sorensen, S.C.: No-flow state following cerebral ischemia. Arch. Neurol. 32, 381–384 (1975)PubMedGoogle Scholar
  7. 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

Copyright information

© Springer-Verlag Berlin · Heidelberg 1976

Authors and Affiliations

  • J. G. Wade
    • 1
  • W. A. Tweed
    • 1
  • W. J. Davidson
    • 1
  1. 1.Department of Anesthesia and Pharmacology and TherapeuticsUniversity of ManitobaWinnipegCanada

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