scholarly journals DEGRADATION KINETICS OF HIGH ENERGY PHOSPHATES IN THE RABBIT BRIN USING NMR-SPECTROSCOPY

1985 ◽  
Vol 19 (10) ◽  
pp. 1073-1073
Author(s):  
N Herschkowitz ◽  
F Stocker ◽  
E Bossi ◽  
M Stoller ◽  
W Aue ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Degradation Kinetics ◽  
High Energy ◽  
High Energy Phosphates ◽  
Kinetics Of

scholarly journals Adenosine attenuates loss of high energy phosphates in ischemic myocardium evaluated by phosphorus NMR spectroscopy

1990 ◽  
Vol 15 (2) ◽  
pp. A208
Author(s):  
Pamela A. Marcovitz ◽  
Alex M. Aisen ◽  
Laura E. Fencil ◽  
Scott D. Swanson ◽  
Andrew J. Buda
Keyword(s):  
Nmr Spectroscopy ◽  
High Energy ◽  
Ischemic Myocardium ◽  
High Energy Phosphates ◽  
Phosphorus Nmr

Time course of myocardial sodium accumulation after burn trauma: a 31P- and 23Na-NMR study

2001 ◽  
Vol 91 (6) ◽  
pp. 2695-2702 ◽  
Author(s):  
Patricia J. Sikes ◽  
Piyu Zhao ◽  
David L. Maass ◽  
Jureta W. Horton
Keyword(s):  
Nmr Spectroscopy ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Intracellular Ph ◽  
Total Body Surface Area ◽  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphates ◽  
Ventricular Performance ◽  
Burn Trauma

In this study,23Na- and 31P- nuclear magnetic resonance (NMR) spectra were examined in perfused rat hearts harvested 1, 2, 4, and 24 h after 40% total body surface area burn trauma and lactated Ringer resuscitation, 4 ml · kg−1 · %−1 burn.23Na-NMR spectroscopy monitored myocardial intracellular Na+ using the paramagnetic shift reagent thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylenephosphonic acid). Left ventricular function, cardiac high-energy phosphates (ATP/PCr), and myocyte intracellular pH were studied by using31P NMR spectroscopy to examine the hypothesis that burn-mediated acidification of cardiomyocytes contributes to subsequent Na+ accumulation by this cell population. Intracellular Na+ accumulation was confirmed by sodium-binding benzofuran isophthalate loading and fluorescence spectroscopy in cardiomyocytes isolated 1, 2, 4, 8, 12, 18, and 24 h postburn. This myocyte Na+ accumulation as early as 2 h postburn occurred despite no changes in cardiac ATP/PCr and intracellular pH. Left ventricular function progressively decreased after burn trauma. Cardiomyocyte Na+ accumulation paralleled cardiac contractile dysfunction, suggesting that myocardial Na+overload contributes, in part, to the progressive postburn decrease in ventricular performance.

Effects of Portal Vein Occlusion on High-Energy Phosphates in Rat Liver Measured by 31P-NMR Spectroscopy

1989 ◽  
Vol 6 (4) ◽  
pp. 176-179 ◽  
Author(s):  
Masahiro Okuda ◽  
Mannosuke Muneyuki ◽  
Yoshifumi Kawarada ◽  
Ryuzi Mizumoto ◽  
Takayuki Sogabe ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Portal Vein ◽  
Rat Liver ◽  
High Energy ◽  
High Energy Phosphates ◽  
Portal Vein Occlusion ◽  
Vein Occlusion

scholarly journals Characterization of Cerebral Energetics and Brain pH by 31P Spectroscopy after Graded Canine Cardiac Arrest and Bypass Reperfusion

1990 ◽  
Vol 10 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Gerard B. Martin ◽  
Richard M. Nowak ◽  
Norman Paradis ◽  
Jack Rosenberg ◽  
Dean Walton ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Nmr Spectroscopy ◽  
Energy State ◽  
High Energy ◽  
Neurologic Outcome ◽  
High Energy Phosphates ◽  
Brain Ph ◽  
Similar Assessment

Recovery of cerebral energy metabolism is used to indicate CNS viability after ischemia. This study utilized 31P nuclear magnetic resonance (NMR) spectroscopy to measure cerebral energy state and intracellular pH in dogs subjected to 8, 12, or 16 min of cardiac arrest and reperfusion using cardiopulmonary bypass. Spectra were obtained throughout ischemia and initial reperfusion and repeated at 30 and 144 h post ischemia. Neurologic deficit scoring was performed at 12 and 24 h post insult and then daily. High-energy phosphates were depleted by the end of all ischemic intervals. Recovery occurred within 60 min of reperfusion and persisted with no differences in the rate of return between groups (p > 0.05). Brain pH (pHb) decreased by the end of ischemia in all groups (p < 0.0001). Neither the pHb nadir nor its recovery differed between groups (p > 0.05). Although long-term neurologic outcome differed between groups, the spectra were similar. Assessment of cerebral energy state using 31P NMR spectroscopy does not appear to be a sensitive indicator of neurologic outcome after global ischemia in dogs. Return of high-energy phosphates may be a necessary but not sufficient condition for cerebral recovery after ischemia. The return of high-energy phosphates after a 16-min cardiac arrest, however, indicates a potential for neurological recovery.

scholarly journals The Flux from Glucose to Glutamate in the Rat Brain in vivo as Determined by 1-Observed, 13C-Edited NMR Spectroscopy

1990 ◽  
Vol 10 (2) ◽  
pp. 170-179 ◽  
Author(s):  
Susan M. Fitzpatrick ◽  
Hoby P. Hetherington ◽  
Kevin L. Behar ◽  
Robert G. Shulman
Keyword(s):  
Steady State ◽  
Nmr Spectroscopy ◽  
Rat Brain ◽  
Tca Cycle ◽  
Difference Spectrum ◽  
Order Rate Constant ◽  
High Energy ◽  
High Energy Phosphates ◽  
Measured Intensity

The rate of incorporation of carbon from [1-13C]glucose into the [4-CH2] and [3-CH2] of cerebral glutamate was measured in the rat brain in vivo by 1H-observed, 13C-edited (POCE) nuclear magnetic resonance (NMR) spectroscopy. Spectra were acquired every 98 s during a 60-min infusion of [1-13C]glucose. Complete time courses were obtained from six animals. The measured intensity of the unresolved [4-13CH2] resonances of glutamate and glutamine increased exponentially during the infusion and attained a steady state in ∼20 min with a first-order rate constant of 0.130 ± 0.010 min−1 (t1/2 = 5.3 ± 0.5 min). The appearance of the [3-13CH2] resonance in the POCE difference spectrum lagged behind that of the [4-13CH2] resonance and had not reached steady state at the end of the 60-min infusion (t1/2 = 26.6 ± 4.1 min). The increase observed in 13C-labeled glutamate represented isotopic enrichment and was not due to a change in the total glutamate concentration. The glucose infusion did not affect the levels of high-energy phosphates or intracellular pH as determined by 31P NMR spectroscopy. Since glucose carbon is incorporated into glutamate by rapid exchange with the tricarboxylic acid (TCA) cycle intermediate α-ketoglutarate, the rate of glutamate labeling provided an estimate of TCA cycle flux. We have determined the flux of carbon through the TCA cycle to be ≈1.4 μmol g−1 min−1. These experiments demonstrate the feasibility of measuring metabolic fluxes in vivo using 13C-labeled glucose and the technique of 1H-observed, 13C-decoupled NMR spectroscopy.

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