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Research Article| Volume 17, ISSUE 4, P256-260, July 1995

Intracellular alkalosis during hypoxia in newborn mouse brain in the presence of systemic acidosis: a phosphorus magnetic resonance spectroscopic study

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      Abstract

      We investigated the in vivo changes in cerebral energy metabolism and pHi in newborn mice noninvasively during 8 h of hypoxia with FiO2 = 5%, using phosphorus magnetic resonance spectroscopy continuously. The intracellular brain pH (pHi) increased from 7.20 ± 0.03 to 7.36 ± 0.03 (P < 0.05) at 1 h of hypoxia and then decreased gradually. On the other hand, the mixed arterial and venous blood pH decreased gradually during hypoxia, reaching a minimum value of 7.16 ± 0.01 at the end of the hypoxia. There was no significant difference in PCO2 between control (47.4 ± 0.8 mm Hg) and 1-h hypoxic (49.0 ± 1.1 mm Hg) mice. The blood glucose concentration was significantly increased at 1 h of hypoxia. These results indicate that the alkaline shift in pHi during hypoxia was caused neither by systemic alkalosis due to hypocapnia nor hypoglycemia.

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      Reference

        • Siesjö B.K.
        Cell damage in the brain: a speculative synthesis.
        J Cereb Blood Flow Metab. 1981; 1: 155-185
        • Paljarvi L.
        • Rehncrona S.
        • Soderfeldt B.
        • Olsson Y.
        • Kalimo H.
        Brain lactic acidosis and ischemic cell damage: Quantitative ultrastructural changes in capillaries of rat cerebral cortex.
        Acta Neuropathol. 1983; 60: 232-240
        • Hillered L.
        • Siesjö B.K.
        • Arfors K.E.
        Mitochondrial response to transient forebrain ischemia and recirculation in the rat.
        J Cereb Blood Flow Metab. 1984; 4: 438-446
        • Siesjö B.K.
        • Bendek G.
        • Koide T.
        • Westerberg E.
        • Wieloch T.
        Influence of acidosis on lipid peroxidation in brain tissues in vitro.
        J Cereb Blood Flow Metab. 1985; 5: 253-258
        • Hasegawa K.
        • Yoshioka H.
        • Sawada T.
        • Nishikawa H.
        Lipid peroxidation in neonatal mouse brain subjected to two different types of hypoxia.
        Brain Dev (Tokyo). 1991; 13: 101-103
        • Siesjö B.K.
        • Ekholm A.
        • Katsura K.
        • Theander S.
        Acid-base changes during complete brain ischemia.
        Stroke. 1990; 21: 194-198
        • Volpe J.J.
        Hypoxic-ischemic encephalopathy. Neuropathology and pathogenesis.
        in: Markowitz M. Watanabe K. Okada S. Neurology of the newborn. WB Saunders Co, Philadelphia1987: 209-235
        • Yoshioka H.
        Neonatal asphyxia and subsequent brain development in the mouse.
        in: Yabuuchi H. Neonatal brain and behavior. Nagoya University Press, Nagoya1987: 27-34
        • Yoshioka H.
        • Iino S.
        • Sato N.
        • et al.
        New model of hemorrhagic hypoxic-ischemic encephalopathy in newborn mice.
        Pediatr Neurol. 1989; 5: 221-225
        • Petroff O.A.C.
        • Prichard J.W.
        • Behar K.L.
        • Alger J.R.
        • den Hollander J.A.
        • Shulman R.G.
        Cerebral intracellular pH by31P nuclear magnetic resonance spectroscopy.
        Neurology. 1985; 35: 781-788
        • Yoshioka H.
        • Fujiwara K.
        • Ishimura K.
        • et al.
        Brain energy metabolism in two kinds of total asphyxia: an in vivo phosphorus nuclear magnetic resonance spectroscopic study.
        Brain Dev (Tokyo). 1988; 10: 88-91
        • Myers R.E.
        Two patterns of perinatal brain damage and their conditions of occurrence.
        Am J Obstet Gynecol. 1972; 15: 246-276
        • Carlsson C.
        • Hagerdal M.
        • Siesjö B.K.
        Protective effect of hypothermia in cerebral oxygen deficiency caused by arterial hypoxia.
        Anesthesiology. 1976; 44: 27-35
        • Hagerdal M.
        • Welsh F.A.
        • Keykhah M.
        • Perez E.
        • Harp J.R.
        Protective effects of combinations of hypothermia and barbiturates in cerebral hypoxia in the rat.
        Anesthesiology. 1978; 49: 165-169
        • Young R.S.K.
        • Olenginski T.P.
        • Yagel S.K.
        • Towfighi J.
        The effect of graded hypothermia on hypoxic-ischemic brain damage: a neuropathologic study in the neonatal rat.
        Stroke. 1983; 14: 929-934
        • Kogure K.
        • Busto R.
        • Schwartzman R.J.
        • Scheinberg P.
        The dissociation of cerebral blood flow, metabolism, and function in the early stages of developing cerebral infarction.
        Ann Neurol. 1980; 8: 278-290
        • Blomqvist P.
        • Mabe H.
        • Siesjö B.K.
        Transient ischemia leads to intracellular alkalosis in the brain.
        Acta Physiol Scand. 1982; 116: 103-114
        • Mabe H.
        • Blomqvist P.
        • Siesjö B.K.
        Intracellular pH in the brain following transient ischemia.
        J Cereb Blood Flow Metab. 1983; 3: 109-114
        • Yoshida S.
        • Busto R.
        • Martinez E.
        • Scheinberg P.
        • Ginsberg M.D.
        Regional brain energy metabolism after complete versus incomplete ischemia in the rat in the absence of severe lactic acidosis.
        J Cereb Blood Flow Metab. 1985; 5: 490-501
        • Syrota A.
        • Samson Y.
        • Boullais C.
        • et al.
        Tomographic mapping of brain intracellular pH and extracellular water space in stroke patients.
        J Cereb Blood Flow Metab. 1985; 5: 358-368
        • Pulsinelli W.A.
        • Brierley J.B.
        • Plum F.
        Temporal profile of neuronal damage in a model of transient forebrain ischemia.
        Ann Neurol. 1982; 11: 491-498
        • Thomas R.C.
        The role of bicarbonate, chloride and sodium ions in the regulation of intracellular pH in snail neurones.
        J Physiol. 1977; 273: 317-338
        • Moody Jr., W.J.
        The ionic mechanism of intracellular pH regulation in crayfish neurones.
        J Physiol. 1981; 316: 293-308
        • Siesjö B.K.
        Acid-base homeostatis in the brain: physiology, chemistry, and neurochemical pathology.
        Prog Brain Res. 1985; 63: 121-154
        • Moor R.D.
        Effects of insulin upon ion transport.
        Biochim Biophys Acta. 1983; 737: 1-49
        • Berridge M.J.
        Inositol triphosphate and diacylglycerol as second messengers.
        Biochem J. 1984; 220: 345-360
        • Cremer J.E.
        • Braun L.D.
        • Oldendorf W.H.
        Changes during development in transport processes of the blood-brain barrier.
        Biochim Biophys Acta. 1976; 448: 633-637
        • Chopp M.
        • Chen H.
        • Vande Linde A.M.Q.
        • Brown E.
        • Welch K.M.A.
        Time course of postischemic intracellular alkalosis reflects the duration of ischemia.
        J Cereb Blood Flow Metab. 1990; 10: 860-865
        • Levine S.R.
        • Welch K.M.A.
        • Bruce R.
        • Smith M.B.
        Brain intracellular pH ‘flip-flop’ in human ischemic stroke identified by31P-NMR.
        Ann Neurol. 1987; 22: 137