Johann Philipp Zöllner1, Elke Hattingen1, Oliver C Singer2, Ulrich Pilatus1. 1. From the Department of Neurology, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany (J.P.Z., O.C.S) and Institute of Neuroradiology, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany (E.H., U.P.). 2. From the Department of Neurology, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany (J.P.Z., O.C.S) and Institute of Neuroradiology, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany (E.H., U.P.). o.singer@em.uni-frankfurt.de.
Abstract
BACKGROUND AND PURPOSE: In vivo changes in tissue pH and energy metabolism are key to understanding stroke pathophysiology. Our goal was to study pH changes in subacute ischemic stroke and their relation to energy metabolism, which, unlike acidosis in acute stroke, are not yet well understood. METHODS: We measured tissue pH and phospholipid as well as cell energy markers, including creatine, phosphocreatine, and N-acetyl-aspartate in subacute stroke with combined (1)H and (31)P magnetic resonance spectroscopy. We included 19 patients with first-ever ischemic stroke (mean time after stroke, 6 days). We then compared metabolite concentrations in the ischemic tissue to contralateral (healthy) tissue using multivariate ANOVA to assess significant differences in metabolite levels between both tissue compartments. RESULTS: In subacute stroke, a tissue fraction with significantly increased tissue pH was observed as compared with healthy contralateral tissue (pH, 7.09 versus 7.03; P=0.002) concurrent with splitting of the pH signal with 1 peak being more alkalotic. Furthermore, only a moderate decrease of energy-rich metabolites (phosphocreatine reduced by 17%, ATP reduced by 19%) was present, whereas total creatine was reduced by 51%. CONCLUSIONS: The finding of an alkalotic pH split in subacute ischemia is unprecedented. The pH split and only incomplete energy loss in subacute stroke suggest 2 differently viable cellular moieties, best explained by active compensatory mechanisms after acute cerebral ischemia.
BACKGROUND AND PURPOSE: In vivo changes in tissue pH and energy metabolism are key to understanding stroke pathophysiology. Our goal was to study pH changes in subacute ischemic stroke and their relation to energy metabolism, which, unlike acidosis in acute stroke, are not yet well understood. METHODS: We measured tissue pH and phospholipid as well as cell energy markers, including creatine, phosphocreatine, and N-acetyl-aspartate in subacute stroke with combined (1)H and (31)P magnetic resonance spectroscopy. We included 19 patients with first-ever ischemic stroke (mean time after stroke, 6 days). We then compared metabolite concentrations in the ischemic tissue to contralateral (healthy) tissue using multivariate ANOVA to assess significant differences in metabolite levels between both tissue compartments. RESULTS: In subacute stroke, a tissue fraction with significantly increased tissue pH was observed as compared with healthy contralateral tissue (pH, 7.09 versus 7.03; P=0.002) concurrent with splitting of the pH signal with 1 peak being more alkalotic. Furthermore, only a moderate decrease of energy-rich metabolites (phosphocreatine reduced by 17%, ATP reduced by 19%) was present, whereas total creatine was reduced by 51%. CONCLUSIONS: The finding of an alkalotic pH split in subacute ischemia is unprecedented. The pH split and only incomplete energy loss in subacute stroke suggest 2 differently viable cellular moieties, best explained by active compensatory mechanisms after acute cerebral ischemia.
Authors: Yunus Msayib; George W J Harston; Kevin J Ray; James R Larkin; Brad A Sutherland; Fintan Sheerin; Nicholas P Blockley; Thomas W Okell; Peter Jezzard; Andrew Baldwin; Nicola R Sibson; James Kennedy; Michael A Chappell Journal: Magn Reson Med Date: 2022-03-07 Impact factor: 3.737
Authors: Matthew G Stovell; Marius O Mada; T Adrian Carpenter; Jiun-Lin Yan; Mathew R Guilfoyle; Ibrahim Jalloh; Karen E Welsh; Adel Helmy; Duncan J Howe; Peter Grice; Andrew Mason; Susan Giorgi-Coll; Clare N Gallagher; Michael P Murphy; David K Menon; Peter J Hutchinson; Keri Lh Carpenter Journal: J Cereb Blood Flow Metab Date: 2018-09-18 Impact factor: 6.200