Advertisement

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

      This paper is only available as a PDF. To read, Please Download here.

      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.

      Keywords

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Brain and Development
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      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