scholarly journals Time Course of Postischemic Intracellular Alkalosis Reflects the Duration of Ischemia

1990 ◽  
Vol 10 (6) ◽  
pp. 860-865 ◽  
Author(s):  
Michael Chopp ◽  
Hua Chen ◽  
Ana M. Q. Vande Linde ◽  
Eileen Brown ◽  
K. M. A. Welch
Keyword(s):  
Specific Gravity ◽  
Brain Tissue ◽  
Cerebral Edema ◽  
Time Course ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Ph Profile ◽  
Tissue Ph ◽  
Tissue Edema

We investigated the long-term (up to 1 week) relationships between the duration of cerebral ischemia and postischemic energy metabolic profile, pH, and tissue edema in the rat. Ten rats each were subjected to 8 or 12 min of forebrain ischemia induced by bicarotid occlusion concurrent with systemic hypotension, and the results were compared with those of 10 sham-operated rat controls. In vivo 31P nuclear magnetic resonance spectroscopy was performed prior to ischemia and at intervals up to 168 h after ischemia. Cerebral edema (measured by specific gravity) was assessed prior to ischemia and at 24, 72, and 168 h after ischemia. The data revealed significant differences in the brain tissue pH profile over time between the ischemic groups (p < 0.03). The 12-min ischemic animals exhibited brain tissue alkalosis (pH = 7.27 ± 0.12) at 24 h compared with both sham (pH = 7.09 ± 0.08) at 24 h and preischemic (pH = 7.06 ± 0.04) pH values. The pH remained alkalotic (pH = 7.23 ± 0.15) through the 48-h time period. In contrast, in the 8-min group, the onset of alkalosis was delayed until 48 h after ischemia (pH = 7.24 ± 0.15), and pH remained alkalotic for only 24 h. No difference in high-energy phosphate metabolism was detected between groups. A different time dependence of tissue pH and specific gravity changes after 12 min of ischemia was detected. The present study suggests that the duration of an ischemic event marks the time of onset of brain tissue alkalosis and its duration and that cerebral edema alone cannot explain the pH changes.

Hepatic phosphate trapping, decreased ATP, and increased feeding after 2,5-anhydro-D-mannitol

1994 ◽  
Vol 266 (1) ◽  
pp. R112-R117 ◽  
Author(s):  
N. E. Rawson ◽  
H. Blum ◽  
M. D. Osbakken ◽  
M. I. Friedman
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Time Course ◽  
Time Frame ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Phosphate Diesters ◽  
Layer Chromatography ◽  
Nuclear Magnetic

The mechanism by which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits feeding behavior was investigated by studying its metabolism and biochemical effects in liver. Thin-layer chromatography of liver extracts from rats given 2,5-AM containing 14C-labeled 2,5-AM showed that the analogue is phosphorylated in vivo with a time course that parallels the eating response. In vivo 31P nuclear magnetic resonance spectroscopy of rat liver during intravenous infusion of 2,5-AM and high-resolution nuclear magnetic resonance analyses of liver extracts showed that 2,5-AM is rapidly phosphorylated in liver, trapping hepatic phosphate and decreasing ATP, inorganic phosphate, and phosphate diesters. These changes occurred in a time frame in which the feeding response is elicited in conscious animals given the same dose of 2,5-AM by the same route. During an interval in which 2,5-AM increased eating, it also increased urinary uric acid excretion, implicating enhanced adenosine degradation in the reduction in hepatic ATP. These results provide the first direct evidence that changes in a high-energy phosphate-carrying compound in liver may provide a signal to initiate eating behavior.

scholarly journals Focal changes in brain energy and phospholipid metabolism in first-episode schizophrenia

2004 ◽  
Vol 184 (5) ◽  
pp. 409-415 ◽  
Author(s):  
J. Eric Jensen ◽  
Jodi Miller ◽  
Peter C. Williamson ◽  
Richard W J. Neufeld ◽  
Ravi S. Menon ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Imaging Techniques ◽  
High Energy ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
First Episode ◽  
Resonance Spectroscopy ◽  
Membrane Breakdown ◽  
First Episode Schizophrenia

BackgroundMembrane phospholipid and high-energy abnormalities measured with phosphorus magnetic resonance spectroscopy (31P-MRS) have been reported in patients with schizophrenia in several brain regions.AimsUsing improved imaging techniques, previously inaccessible brain regions were examined in patients with first-episode schizophrenia and healthy volunteers with 4.0 T 31P-MRS.MethodBrain spectra were collected in vivo from 15 patients with first-episode schizophrenia and 15 healthy volunteers from 15 cm3 effective voxels in the thalamus, cerebellum, hippocampus, anterior/posterior cingulate, prefrontal cortex and parieto-occipital cortex.ResultsPeople with first-episode schizophrenia showed increased levels of glycerophosphocholine in the anterior cingulate. Inorganic phosphate, phosphocreatine and adenosine triphosphate concentrations were also increased in the anterior cingulate in this group.ConclusionsThe increased phosphodiester and high-energy phosphate levels in the anterior cingulate of brains of people with first-episode schizophrenia may indicate neural overactivity in this region during the early stages of the illness, resulting in increased excitotoxic neural membrane breakdown.

scholarly journals Regulation of murine myocardial energy metabolism during adrenergic stress studied by in vivo 31P NMR spectroscopy

2003 ◽  
Vol 285 (5) ◽  
pp. H1976-H1979 ◽  
Author(s):  
A. V. Naumova ◽  
R. G. Weiss ◽  
V. P. Chacko
Keyword(s):  
Heart Rate ◽  
Cardiac Metabolism ◽  
High Energy ◽  
Dobutamine Stress ◽  
Resonance Spectroscopy ◽  
31P Nmr Spectroscopy ◽  
Adult Mice ◽  
The Mean ◽  
Large Animals

Image-guided, spatially localized 31P magnetic resonance spectroscopy (MRS) was used to study in vivo murine cardiac metabolism under resting and dobutamine-induced stress conditions. Intravenous dobutamine infusion (24 μg · min–1 · kg body wt–1) increased the mean heart rate by ∼39% from 482 ± 46 per min at baseline to 669 ± 77 per min in adult mice. The myocardial phosphocreatine (PCr)-to-ATP (PCr/ATP) ratio remained unchanged at 2.1 ± 0.5 during dobutamine stress, compared with baseline conditions. Therefore, we conclude that a significant increase in heart rate does not result in a decline in the in vivo murine cardiac PCr/ATP ratio. These observations in very small mammals, viz., mice, at extremely high heart rates are consistent with studies in large animals demonstrating that global levels of high-energy phosphate metabolites do not regulate in vivo myocardial metabolism during physiologically relevant increases in cardiac work.

scholarly journals Cortical Substrate Oxidation during Hyperketonemia in the Fasted Anesthetized Rat in Vivo

2011 ◽  
Vol 31 (12) ◽  
pp. 2313-2323 ◽  
Author(s):  
Lihong Jiang ◽  
Graeme F Mason ◽  
Douglas L Rothman ◽  
Robin A de Graaf ◽  
Kevin L Behar
Keyword(s):  
Time Course ◽  
Ketone Bodies ◽  
Tricarboxylic Acid Cycle ◽  
Metabolic Model ◽  
Substrate Oxidation ◽  
Resonance Spectroscopy ◽  
Neural Function ◽  
Anesthetized Rats ◽  
Time Courses

Ketone bodies are important alternate brain fuels, but their capacity to replace glucose and support neural function is unclear. In this study, the contributions of ketone bodies and glucose to cerebral cortical metabolism were measured in vivo in halothane-anesthetized rats fasted for 36 hours ( n=6) and receiving intravenous [2,4-13C2]-d- β-hydroxybutyrate (BHB). Time courses of 13C-enriched brain amino acids (glutamate-C4, glutamine-C4, and glutamate and glutamine-C3) were measured at 9.4 Tesla using spatially localized 1H-[13C]-nuclear magnetic resonance spectroscopy. Metabolic rates were estimated by fitting a constrained, two-compartment (neuron–astrocyte) metabolic model to the 13C time-course data. We found that ketone body oxidation was substantial, accounting for 40% of total substrate oxidation (glucose plus ketone bodies) by neurons and astrocytes. d- β-Hydroxybutyrate was oxidized to a greater extent in neurons than in astrocytes (∼70:30), and followed a pattern closely similar to the metabolism of [1-13C]glucose reported in previous studies. Total neuronal tricarboxylic acid cycle (TCA) flux in hyperketonemic rats was similar to values reported for normal (nonketotic) anesthetized rats infused with [1-13C]glucose, but neuronal glucose oxidation was 40% to 50% lower, indicating that ketone bodies had compensated for the reduction in glucose use.

Efficacy of recombinant human Hb by31P-NMR during isovolemic total exchange transfusion

1999 ◽  
Vol 86 (3) ◽  
pp. 887-894 ◽  
Author(s):  
Laurel O. Sillerud ◽  
Arvind Caprihan ◽  
Nancy Berton ◽  
Gary J. Rosenthal
Keyword(s):  
Exchange Transfusion ◽  
High Energy ◽  
Surface Coil ◽  
High Energy Phosphates ◽  
Significant Drop ◽  
Tissue Ph ◽  
Hb Concentration ◽  
Menten Constant ◽  
Total Exchange

The ability of recombinant human Hb (rHb1.1), which is being developed as an oxygen therapeutic, to support metabolism was measured by in vivo31P-NMR surface coil spectroscopy of the rat abdomen in control animals and in animals subjected to isovolemic exchange transfusion to hematocrit of <3% with human serum albumin or 5 g/dl rHb1.1. No significant changes in metabolite levels were observed in control animals for up to 6 h. The albumin-exchange experiments, however, resulted in a more than eightfold increase in Pi and a 50% drop in phosphocreatine and ATP within 40 min. The tissue pH dropped from 7.4 to 6.8. The decrease in high-energy phosphates obeyed Michaelis-Menten kinetics, with a Michaelis-Menten constant of 3% as the hematocrit at which a 50% drop in high-energy phosphates was observed. Exchange transfusion with rHb1.1 resulted in no significant drop in high-energy phosphates, no rise in Pi, and no change in tissue pH from 7.35 ± 0.15 for up to 5 h after exchange. By these criteria, rHb1.1 at a plasma Hb concentration of ∼5 g/dl after total exchange transfusion was able to sustain energy metabolism of gut tissue at levels indistinguishable from control rats with a threefold higher total Hb level in erythrocytes.

Hypoxic pHi and function modulation by Na+/H+ exchange and alpha-adrenoreceptor inhibition in heart in vivo

1997 ◽  
Vol 272 (6) ◽  
pp. H2664-H2670 ◽  
Author(s):  
M. A. Portman ◽  
Y. Xiao ◽  
B. G. Broers ◽  
X. H. Ning
Keyword(s):  
Cardiac Function ◽  
Contractile Function ◽  
High Energy ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Cardiac Contractile Function ◽  
Significant Drop ◽  
And Function ◽  
Phi Regulation

Regulation of intracellular pH (pHi) may contribute to maintenance of cardiac contractile function during graded hypoxia in vivo. To test this hypothesis, we disturbed pHi regulation in vivo using two approaches: alpha-adrenoreceptor antagonism with phentolamine (1 mg/kg) (Phen; n = 9); and Na+/H+ exchange inhibition with HOE-642 (2 mg/kg; n = 6) before graded hypoxia in open-chest sheep. Hemodynamic parameters including left ventricular maximal pressure development (dP/dtmax) cardiac index (CI), and left ventricular power were monitored continuously and simultaneously with high-energy phosphate levels and pHi, measured with 31P nuclear magnetic resonance spectroscopy in Phen, HOE-642, and control (Con; n = 9). In subgroups (n = 6) in Con and Phen, coronary flow, myocardial oxygen consumption (MVO2), and lactate uptake were also measured. During hypoxia, the functional parameters left ventricular dP/dtmax, CI, and left ventricular power decreased significantly compared with baseline and Con values. These decreases were preceded by a significant drop (P < 0.05) in pHi from 7.10 +/- 0.04 to 6.69 +/- 0.05 in Phen and corresponded temporally to a pHi drop from 7.10 +/- 0.02 to 6.77 +/- 0.03 in HOE-642. Decreases in pHi in Phen were not preceded by decreases in cardiac function or MVO2. In contrast, cardiac function parameters increased significantly in Con, whereas no significant pHi decrease occurred (7.07 +/- 0.03 to 6.98 +/- 0.04). We conclude that these data indicate that pHi regulation can be disrupted through alpha-adrenergic antagonism or Na+/H(+)-exchange inhibition in vivo. These studies demonstrate that pHi regulation performs a role in the modulation of cardiac function during hypoxia in vivo.

In vitro and in vivo measurements of fiber optic and electrochemical sensors to monitor brain tissue pH

2001 ◽  
Vol 72 (2) ◽  
pp. 174-179 ◽  
Author(s):  
Sheila A. Grant ◽  
Kerry Bettencourt ◽  
Peter Krulevitch ◽  
Julie Hamilton ◽  
Robert Glass
Keyword(s):  
Brain Tissue ◽  
Electrochemical Sensors ◽  
Fiber Optic ◽  
Tissue Ph ◽  
In Vivo Measurements
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