scholarly journals Phosphorus spectroscopy in acute TBI demonstrates metabolic changes that relate to outcome in the presence of normal structural MRI

2018 ◽  
Vol 40 (1) ◽  
pp. 67-84
Author(s):  
Matthew G Stovell ◽  
Marius O Mada ◽  
T Adrian Carpenter ◽  
Jiun-Lin Yan ◽  
Mathew R Guilfoyle ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracellular Ph ◽  
Acute Phase ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
Unfavourable Outcome ◽  
Visible Injury ◽  
Monitoring Therapy ◽  
Significant Difference

Metabolic dysfunction is a key pathophysiological process in the acute phase of traumatic brain injury (TBI). Although changes in brain glucose metabolism and extracellular lactate/pyruvate ratio are well known, it was hitherto unknown whether these translate to downstream changes in ATP metabolism and intracellular pH. We have performed the first clinical voxel-based in vivo phosphorus magnetic resonance spectroscopy (31P MRS) in 13 acute-phase major TBI patients versus 10 healthy controls (HCs), at 3T, focusing on eight central 2.5 × 2.5 × 2.5 cm3 voxels per subject. PCr/γATP ratio (a measure of energy status) in TBI patients was significantly higher (median = 1.09) than that of HCs (median = 0.93) (p < 0.0001), due to changes in both PCr and ATP. There was no significant difference in PCr/γATP between TBI patients with favourable and unfavourable outcome. Cerebral intracellular pH of TBI patients was significantly higher (median = 7.04) than that of HCs (median = 7.00) (p = 0.04). Alkalosis was limited to patients with unfavourable outcome (median = 7.07) (p < 0.0001). These changes persisted after excluding voxels with > 5% radiologically visible injury. This is the first clinical demonstration of brain alkalosis and elevated PCr/γATP ratio acutely after major TBI. 31P MRS has potential for non-invasively assessing brain injury in the absence of structural injury, predicting outcome and monitoring therapy response.

scholarly journals Brain Injury and Recovery Following Binge Ethanol: Evidence from In Vivo Magnetic Resonance Spectroscopy

2010 ◽  
Vol 67 (9) ◽  
pp. 846-854 ◽  
Author(s):  
Natalie M. Zahr ◽  
Dirk Mayer ◽  
Torsten Rohlfing ◽  
Michael P. Hasak ◽  
Oliver Hsu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Resonance Spectroscopy ◽  
Binge Ethanol

A FRET-based two-photon probe for in vivo tracking of pH during a traumatic brain injury process

2019 ◽  
Vol 43 (43) ◽  
pp. 17018-17022
Author(s):  
Baoping Zhai ◽  
Shuyang Zhai ◽  
Ruilin Hao ◽  
Jianjun Xu ◽  
Zhihong Liu
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurodegenerative Diseases ◽  
Intracellular Ph ◽  
Ph Change ◽  
Ph Probe ◽  
Two Photon ◽  
Ph Decrease

Traumatic brain injury (TBI) is a cause of neurodegenerative diseases accompanied by intracellular pH decrease. Herein, a FRET-based ratiometric two-photon fluorescent pH probe is designed to monitor pH change and understand TBI process.

Diaphragmatic fatigue assessed by 31P-magnetic resonance spectroscopy in vivo

1993 ◽  
Vol 264 (5) ◽  
pp. C1111-C1118 ◽  
Author(s):  
D. G. Nichols ◽  
J. R. Buck ◽  
S. M. Eleff ◽  
D. C. Shungu ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Intracellular Ph ◽  
Oxidative Metabolism ◽  
Compound Action Potential ◽  
Separate Group ◽  
Resonance Spectroscopy ◽  
Transdiaphragmatic Pressure ◽  
Control Value

We tested whether fatigue of the piglet diaphragm is associated with inadequate oxidative metabolism as measured by magnetic resonance spectroscopy (MRS). An MRS measured ratio of inorganic phosphate to phosphocreatine (Pi/PCr) > or = 1 was taken as evidence of inadequate oxidative metabolism. Piglets (n = 10) underwent phrenic nerve pacing for 90 min with stimulation frequency of 30 Hz and duty cycle of 0.33. In a separate group of six piglets PCr, Pi, ATP, and intracellular pH were measured by in vivo MRS, and diaphragmatic blood flow was measured with radioactive microspheres at control, 2, 10, 45, 60, and 90 min of pacing. Transdiaphragmatic pressure fell from 25 +/- 3 to 15 +/- 2 mmHg (61 +/- 5%) at 2 min and remained depressed in a separate group of four piglets (P < 0.05). Conversely, compound action potential amplitude remained constant for the first 10 min of pacing and fell to 68 +/- 5% of control at 45 min (P < 0.05). Pi/PCr rose from a control value of 0.32 +/- 0.06 to 0.92 +/- 0.23 at 2 min and 0.79 +/- 0.03 at 10 min (P < 0.05) before returning toward control at 45-90 min. O2 delivery increased from 4.6 +/- 1.2 to 24.7 +/- 4.8 ml.min-1.100 g-1 at 2 min and 18.4 +/- 2.2 ml.min-1.100 g-1 at 10 min (P < 0.05) but then fell to lower levels at 45-90 min. ATP and intracellular pH remained constant except for a decline in pH to 6.98 +/- 0.09 at 45 min (P < 0.05) from the control value of 7.26 +/- 0.06.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic heat improves mechanical and metabolic response of trained rat heart on ischemia and reperfusion

1997 ◽  
Vol 272 (5) ◽  
pp. H2085-H2094 ◽  
Author(s):  
E. Levy ◽  
Y. Hasin ◽  
G. Navon ◽  
M. Horowitz
Keyword(s):  
Oxygen Consumption ◽  
Intracellular Ph ◽  
Cardiac Mechanics ◽  
Heat Acclimation ◽  
High Energy ◽  
Rate Pressure Product ◽  
Resonance Spectroscopy ◽  
Ischemia And Reperfusion ◽  
Swimming Training ◽  
Significant Difference

Cardiac mechanics and metabolic performance were studied in isolated perfused hearts of rats subjected to a combined chronic stress of heat acclimation and swimming training (EXAC) or swimming training alone (EX). Diastolic (DP) and systolic pressures (SP), coronary flow (CF), and oxygen consumption were measured during normoperfusion (80 mmHg), and the appearance of ischemic contracture (IC), DP, and SP were measured during progressive graded ischemia, total ischemia (TI), and reperfusion insults. ATP, phosphocreatine, and intracellular pH were measured during TI and reperfusion with 31P nuclear magnetic resonance spectroscopy. During normoperfusion, SP and cardiac efficiency (derived from rate-pressure product-oxygen consumption relationships) were the highest in the 2-mo EXAC hearts (P < 0.0001). During progressive graded ischemia, the development of IC (percentage of total hearts) was similar in both EXAC and EX hearts; the only significant difference was confined to the 1- vs. 2-mo groups. The onset of IC was delayed in the EXAC hearts and, on reperfusion, recovery, particularly of DP, was significantly improved in the latter. After TI, EXAC hearts retained 30% of the ATP pool and there was a delayed decline in intracellular pH. On reperfusion, these hearts also displayed improved ATP and phosphocreatine recovery, the 2-mo EXAC heart demonstrating significantly faster high-energy phosphate salvage, improved diastolic function, and pulse pressure recovery. The data attest to the beneficial effects of heat acclimation on cardiac mechanics of trained rats during normoperfusion and cardiac protection on ischemia and reperfusion. Possibly, energy sparing, lesser acidosis, and shorter duration of IC on ischemia and improved energy salvage on reperfusion contribute synergistically to this potent beneficial effect.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of insulin on intracellular pH and phosphate metabolism in human skeletal muscle in vivo

1991 ◽  
Vol 81 (1) ◽  
pp. 123-128 ◽  
Author(s):  
D. J. Taylor ◽  
S. W. Coppack ◽  
T. A. D. Cadoux-Hudson ◽  
G. J. Kemp ◽  
G. K. Radda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Inorganic Phosphate ◽  
Human Skeletal Muscle ◽  
Muscle Metabolism ◽  
Normal Subjects ◽  
Phosphate Concentration ◽  
Resonance Spectroscopy ◽  
Phosphorus Containing

1. 31P nuclear magnetic resonance spectroscopy and the hyperinsulinaemic-euglycaemic clamp were used simultaneously to assess the effect of insulin on intracellular pH and the major phosphorus-containing metabolites of normal human skeletal muscle in vivo in four normal subjects. 2. Insulin and glucose were infused for 120 min. Plasma insulin increased approximately 10-fold over pre-clamp levels (5.6 ± 0.9 m-units/l pre-clamp and 54 ± 5 m-units/l over the last hour of infusion; mean ± sem, n = 4). Plasma glucose concentration did not change significantly (5.4 ± 0.2 mmol/l pre-clamp and 5.5 ± 0.1 mmol/l over the last hour of infusion). 3. Insulin and glucose infusion resulted in a decline in the intracellular pH of forearm muscle of 0.027 ± 0.007 unit/h (P < 0.01), whereas in control studies of the same subjects, pH rose by 0.046 ± 0.005 unit/h (P < 0.001). 4. In the clamp studies, intracellular inorganic phosphate concentration rose by 18%/h, whereas ATP, phosphocreatine and phosphomonoester concentrations did not change. In plasma, inorganic phosphate concentration was 1.16 ± 0.05 mmol/l before infusion, and this decreased by a mean rate of 0.14 mmol h−1 l−1. No change was observed in any of these intracellular metabolites in the control studies. 5. The results show that, under physiological conditions, insulin does not raise intracellular pH in human muscle, and thus cannot influence muscle metabolism by this mechanism. The results also suggest that insulin causes a primary increase in the next flux of inorganic phosphate across the muscle cell membrane.

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