Abstract
During arterial hypoxia the brain blood flow rate increases when oxygen tensions below approximately 60 mmHg are attained (Betz, 1972; Grote and Schubert, 1982; Kuschinsky, and Wahl, 1978). Tissue PO2 measurements as well as tissue metabolite assays performed under the same conditions indicate the existence of pronounced tissue hypoxia and the beginning of hypoxic changes in brain metabolism (Grote, Zimmer and Schubert, 1981). Possible mediators of hypoxia-induced cerebral vasodilatation are various metabolic factors, the concentrations of which increase under conditions of insufficient brain oxygen supply. Among these vasodilating factors, potassium and hydrogen ions as well as adenosine seem to play an important role (Betz, 1972; Kuschinsky and Wahl, 1978; Rubio et al., 1985). Different additional vasoactive substances released at low oxygen tensions by the tissue or by the vessel wall itself, especially by the endothelium, are under investigation (Busse et al., 1984; Coburn et al., 1979; Detar, 1980; Eckenfels and Vane, 1972; Fay, 1971; Furchgott and Zawadzki, 1980; Pitman and Duling, 1973; Rubanyi and Vanhoutte, 1985; Rubio et al., 1975; Sparks, Jr. 1980; Vanhoutte, 1976).
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© 1988 Plenum Press, New York
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Grote, J., Siegel, G., Zimmer, K., Adler, A. (1988). The Influence of Oxygen Tension on Membrane Potential and Tone of Canine Carotid Artery Smooth Muscle. In: Mochizuki, M., Honig, C.R., Koyama, T., Goldstick, T.K., Bruley, D.F. (eds) Oxygen Transport to Tissue X. Advances in Experimental Medicine and Biology, vol 222. Springer, New York, NY. https://doi.org/10.1007/978-1-4615-9510-6_57
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