Cerebral intracellular pH by
            <sup>31</sup>
            P nuclear magnetic resonance spectroscopy

Petroff, Ognen A. C.; Prichard, James W.; Behar, Kevin L.; Alger, J. R.; Hollander, Jan A. den; Shulman, Robert G.

doi:10.1212/wnl.35.6.781

Cited by 516 publications

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“…Linear baseline corrections in spectral sections around each of the resonances were applied before the peak po sitions and areas were evaluated with a line fitting rou tine. The chemical shift difference (8, in ppm) of the Pi peak relative to the PCr peak was related to the intracel lular brain pH (Petroff et a!., 1985) by the equation pH = 6.77 + log[(8-3.29)/(5. 68-8)].…”

Section: Physiological Monitoringmentioning

confidence: 99%

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Widmer

Abiko

Faden

et al. 1992

J Cereb Blood Flow Metab

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Summary:The effects of hyperglycemia on the time course of changes in cerebral energy metabolite concen trations and intracellular pH were measured by nuclear magnetic resonance (NMR) spectroscopy in rats sub jected to temporary complete brain ischemia. Interleaved 31p and IH NMR spectra were obtained every 5 min be fore, during, and for 2 h after a 30-min bilateral carotid occlusion preceded by permanent occlusion of the basilar artery. The findings were compared with free fatty acid and excitatory amino acid levels as well as with cations and water content in funnel-frozen brain specimens. One hour before occlusion, nine rats received 50% glucose (12 mJJkg i.p.) and five received 7% saline (12 mllkg i.p.). Before ischemia, there were no differences in cerebral metabolite levels or pH between hyperglycemic rats and controls. During the carotid occlusion, the lactatelN acetylaspartate (Lac/NAA) peak ratio was higher (0.73- 456phate were totally depleted in both groups. Within 5-15 min after the onset of reperfusion, the LaclNAA peak ratio increased further in all rats; however, only in ex tremely hyperglycemic rats (serum glucose> 960 mg/dl) did the lactic acidosis progress rather than recover later during reperfusion. Total free fatty acid and excitatory amino acid levels, but not cation concentration or water content, in brain correlated with serum glucose levels during and after ischemia and with NMR findings after 2 h of reperfusion. Although profound hyperglycemia (se rum glucose of 970-1 ,650 mg/dl) appears to be associated with progression of anaerobic glycolysis and failure of cerebral energy metabolism to recover after temporary complete brain ischemia and with postischemic excito toxic and lipolytic reactions thought to participate in de layed cellular injury, severe hyperglycemia (490-720 mg/ dl) was associated with recovery of energy metabolism.

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Section: Physiological Monitoringmentioning

confidence: 99%

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Widmer

Abiko

Faden

et al. 1992

J Cereb Blood Flow Metab

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“…Linewidth variations were assumed to be negligi ble. The pH was determined using the frequency differ ence between the inorganic phosphate Pi and the PCr signals and a titration curve established by Petroff et al (1985), assuming the frequency differences are not af fected by rapid pUlsing. In the later stages of ischemia, when the PCr was not present, its frequency for the pur pose of pH determination was taken to be unchanged from its position in the last spectrum in which it was present.…”

Section: Nmr Data Analysismentioning

confidence: 99%

Assessment of Postischemic Cerebral Energy Metabolism in Cat by ³¹P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia

Alger

Brunetti²,

Nagashima

et al. 1989

J Cereb Blood Flow Metab

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Summary:The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cere bral ischemia was evaluated in a cat model using 31p nu clear magnetic resonance (NMR) spectroscopic methods.Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial oc clusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severeIn experimental models of recovery from cerebral ischemia, a brief period of reactive hyperemia is followed by long-lasting postischemic deficits in ce rebral blood flow (Hossmann et aI. , 1973; Levy et aI., 1979; Pulsinelli et aI., 1982; Kagstr6m et aI., 1983; Suzuki et aI., 1983). The pathophysiological processes that lead to postischemic hypoperfusion, while not clearly understood, seem to be related to an increased vascular tone (Schmidt-Kastner et aI., 1987). During the hypoperfusion phase, there is a lack of CO2 reactivity, indicating an uncoupling of cerebral blood flow and metabolic activity (Hoss mann et aI., 1973; Snyder et aI., 1975). For this reason, the brain may exhibit postischemic hyper sensitivity to additional hypoxic-ischemic stress, even if the levels of energy-yielding phosphates are 506energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phos phocreatine and intracellular inorganic phosphate, which were slightly amplified in animals that previously experi enced ischemia. Key Words: Cerebral ischemia-Energy metabolism-31 P NMR-Hypoxia-Cat.replenished to normal before the secondary injury occurs. Such a postischemic metabolic hypersensi tivity to stress may be relevant, as suggested by a recent study (Tomida et aI., 1987) of repetitive ce rebral ischemia in gerbils, where animals receiving brief secondary and tertiary ischemic injuries were found to have a higher morbidity and were more prone to develop cerebral edema than animals ex periencing a single long ischemic episode.The present study was designed to evaluate the metabolic consequences of postischemic hypoper fusion in cats receiving repetitive ischemic injuries. In particular, it addresses the questions of how quickly metabolic parameters (high energy phos phates and pH) recover after ischemia, and whether hypoxic or further ischemic injuries result in a more serious decline or a slower recovery of these pa rameters. 31 P nuclear magnetic resonance (NMR) spectroscopy was chosen as the primary experi mental technique, because it is rapidly being ac cepted as a useful method for repetitive noninvasive measurements of cerebral energy status and intra cellular pH (for review, see Prichard and Shulman, 1986). The cat model was given preference to a ro dent model, because the physiologic state can be better controlled, and because the larger brain of-

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“…Free intracellular inorganic phosphates constitute the Pi resonance [20] and is produced from ATP which hydrolyzes to ADP and Pi, liberating large amount of free energy for cell functions [12]. This was found to be increased in conditions of hypoxia [21].…”

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confidence: 99%

Energy Status And Metabolism in Intracranial Space Occupying Lesions: A Prospective 31p Spectroscopic Study

Kamble¹

2014

JCDR

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Aim: Intracranial space occupying lesions can be infective or tumour. There are various advanced Magnetic resonance imaging techniques like perfusion, diffusion and proton spectroscopy which can differentiate between them. However, 31 Phosphorus spectroscopy studies the energy status and the metabolism pattern of various tissues and can be used potentially to differentiate between them depending on their Metabolism pattern. Thus, we aimed to study energy status of various intracranial lesions and try to differentiate between them including grades of gliomas. Materials and Methods:31 PMRS was done in 1.5T MRI in 43 patients prior to surgery or through/via stereo-tactic biopsy, of which 25 were men and 18 women with mean age 41.34 y ranging from 7-71 y. Single voxel phosphorus spectroscopy was done from the solid portion of the lesions and data was analysed and post processed.Results: Study includes Lymphoma (n=6), Grade 1 and 2 glioma (n=5), grade 3 glioma (n=9), grade 4 glioma(n=6), metastases (n=5), tuberculoma (n=7) and pyogenic abscesses (n=5). The integral values of PME, Pi, PDE, γ-ATP, α-ATP, β-ATP with reference to the position of PCr were calculated along with various ratios. Integral values of Pi and PDE were significantly increased in metastases but decreased in gliomas grade 1-2 compared to other pathologic conditions. Mean integral values of LEP (low energy phosphates) and total phosphates were significantly decreased in gliomas grades 1 and 2 and increased in metastases when compared with other pathologic conditions. PCr /Pi was increased in glioma grades 1, 2 and 3 but decreased in metastases; the significance was observed only in gliomas grade 3 and metastases. Metabolic ratios of PDE/βATP and Pi/ βATP were decreased in glioma grades 1 and 2 and increased in metastases with statistical significance. Conclusion:31 PMRS may help in differentiating primary from secondary lesions and assess grades of gliomas. P MR spectroscopy (TR = 400ms, TE=1ms, 512 acquisitions) using intravoxel in-vivo spectroscopy localization method with head quadrature dual-tuned coil. Care was taken to include mainly the solid portion of the lesion in the MRS voxel which ranged from 2 cm 3 -4 cm 3 . The duration of spectroscopy examination was about 5 min. Spectroscopy data were transferred to an installed software programme (Numaris spectroscopy analysis package VB33A). All post-processing techniques like apodization, zero and first order phase corrections were performed and spectra were plotted, analyzed and fitted to Lorentzian lines shapes.The following well resolved phosphorus metabolite peaks were observed in all patients-Phosphomonoesters (PME), Inorganic phosphate (Pi), Phosphodiesters (PDE), Phosphocreatine (PCr), γ, β, and α resonances of adenosine triphosphate (ATP). The chemical

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Cerebral intracellular pH by ³¹ P nuclear magnetic resonance spectroscopy

Cited by 516 publications

References 0 publications

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Assessment of Postischemic Cerebral Energy Metabolism in Cat by ³¹P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia

Energy Status And Metabolism in Intracranial Space Occupying Lesions: A Prospective 31p Spectroscopic Study

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Cerebral intracellular pH by 31 P nuclear magnetic resonance spectroscopy

Cited by 516 publications

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Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of1H and31P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of1H and31P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Assessment of Postischemic Cerebral Energy Metabolism in Cat by 31P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia

Energy Status And Metabolism in Intracranial Space Occupying Lesions: A Prospective 31p Spectroscopic Study

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Cerebral intracellular pH by ³¹ P nuclear magnetic resonance spectroscopy

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of¹H and³¹P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

Assessment of Postischemic Cerebral Energy Metabolism in Cat by ³¹P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia