Abstract
Stroke is most often due to the occlusion of a single intracranial artery, resulting in incomplete focal ischemia. This has an immediate deleterious effect upon cerebral energy metabolism and dependent processes (Lowry and Passonneau, 1964). There is a rapid decrease of high-energy phosphate intermediates, a shift toward reduction of mitochondrial respiratory chain metabolites, increased lactic acid, and acidosis in the ischemic focus (Goldberg et al., 1966; Michenfelder and Theye, 1970). Most investigators have considered that acidosis causes or contributes in a major way to cellular damage in ischemic brain (for a review, see Welch and Barkley [1986]). In recent clinical studies of acute focal ischemic stroke, using the capability of 31p nuclear magnetic resonance spectroscopy (NMRS) to dynamically measure the brain intracellular pH, we observed a transition from acidosis to alkalosis in ischemic brain as early as 18 hr after the onset of stroke (Levine et al., 1987). Positron emission tomography (PET) has corroborated the finding of alkalosis in clinical studies of subacute and late focal ischemic stroke (Syrota et al., 1985; Hakim et al., 1987). A rapid transition from acidosis to alkalosis has also been observed in experimental stroke models of either focal or global complete or incomplete ischemia, with or without reperfusion (Kogure et al., 1980; Mabe et al., 1983; Paschen et al., 1985; Yoshida et al., 1985). In this chapter we explore in clinical patients with cerebral ischemia (1) the significance of brain acidosis and (2) the currently unknown mechanisms and meaning of what we have termed the acid-to-base pH “flip-flop.”
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Welch, K.M.A., Levine, S.R., Martin, G.B., Helpern, J.A. (1992). Cellular and Metabolic Significance of Cellular Acid-Base Shifts in Human Stroke. In: Bazan, N.G., Braquet, P., Ginsberg, M.D. (eds) Neurochemical Correlates of Cerebral Ischemia. Advances in Neurochemistry, vol 7. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3312-2_17
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DOI: https://doi.org/10.1007/978-1-4615-3312-2_17
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