Abstract
Ischemic attacks cause drastic vasodilatation in the brain circulation and subsequent hyperemia. Simultaneously the regulation of regional cerebral blood flow is impaired or abolished. Following cerebral ischemia, arterial hypercapnia (Yamaguchi et al. 1972; Seki et al. 1984) and changes in the concentrations of various vasoactive substances in the perivascular space have little or no effect on brain vessel diameter (Berne et al. 1974; Harris and Symon 1984; Strong et al. 1988). During microapplication studies on pial arteries a reduction of the reactivity to local metabolic factors such as H+ and K+ was observed (Haller and Kuschinsky 1981; Haller et al. 1986). As a consequence of the postischemic disturbance in cerebrovascular reactivity, an impaired adjustment of cerebral blood flow to the metabolic demand has to be expected.
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© 1989 Springer-Verlag Berlin Heidelberg
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Hagendorff, A. et al. (1989). The Effects of Transient and Long-Term Ischemia on Tissue PO2 in the Brain Cortex. In: Hartmann, A., Kuschinsky, W. (eds) Cerebral Ischemia and Calcium. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85863-5_14
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DOI: https://doi.org/10.1007/978-3-642-85863-5_14
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