High‐Energy Phosphate Metabolism during Exercise and Recovery in Temperate and Antarctic Scallops: An In Vivo 31P‐NMR Study

2003 ◽  
Vol 76 (5) ◽  
pp. 622-633 ◽  
Author(s):  
David M. Bailey ◽  
Lloyd S. Peck ◽  
Christian Bock ◽  
Hans‐Otto Pörtner
Keyword(s):  
31P Nmr ◽  
High Energy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
Nmr Study ◽  
High Energy Phosphate Metabolism

Myocardial high-energy phosphate metabolism is altered after treatment with anthracycline in childhood

2000 ◽  
Vol 10 (6) ◽  
pp. 610-617 ◽  
Author(s):  
Andrea B. Eidenschink ◽  
Gerrit Schröter ◽  
Stefan Müller-Weihrich ◽  
Heiko Stern
Keyword(s):  
Adenosine Triphosphate ◽  
High Energy ◽  
Left Ventricular ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
Resonance Spectroscopy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
High Energy Phosphate Metabolism

AbstractObjectivesWe aimed to investigate whether changes in high-energy phosphate metabolism after treatment of children and young adults with anthracycline can be demonstrated non-invasively by 31P magnetic resonance spectroscopy.BackgroundAbnormal myocardial energy metabolism has been suggested as a mechanism for anthracycline-induced cardiotoxicity. Deterioration in such has been shown in animal studies by resonance spectroscopy.MethodsWe studied 62 patients, with a mean age of 13.5 ±5 years,3.7±4.3 years after a cumulative anthracycline dose of 270±137 mg/m2. Normal echocardiographic findings had been elicited in 54 patients. The control group consisted of 28 healthy subjects aged 20±7 years. Resonance spectrums of the anterior left ventricular myocardium were obtained at 1.5 Tesla using an image-selected in vivo spectroscopy localization technique.ResultsThe ratio of phosphocreatine to adenosine triphosphate after blood correction was 1.09±0.43 for the patients, and 1.36±0.36 (mean±SD)for controls (p = 0.005), with a significantly reducedmean ratio even in the subgroup of patients with normal echocardiographic results ( l.11 ± 0. 44 versus1.36±0.36, p=0.01). The ratio did not correlate with the cumulative dose of anthracycline. The ratio of phosphodiester to adenosine triphosphate was similar in patients and controls (0.90±0.56 versus 0.88±0.62).ConclusionsIn patients treated with anthracyclines in childhood, myocardial high-energy phosphate metabolism may be impaired even in the absence of cardiomyopathy. Our data support the concept that anthracycline-induced cardiotoxicity is not clearly dose dependent.

In vivo 31 P-NMR studies of myocardial high energy phosphate metabolism during anoxia and recovery

FEBS Letters ◽  
1983 ◽  
Vol 159 (1-2) ◽  
pp. 207-210 ◽  
Author(s):  
Klaus J. Neurohr ◽  
Gerald Gollin ◽  
Eugene J. Barrett ◽  
Robert G. Shulman
Keyword(s):  
High Energy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
Nmr Studies ◽  
High Energy Phosphate Metabolism

Brain High Energy Phosphate Responses to Alcohol Exposure in Neonatal Rats: An In Vivo 31P-NMR Study

2000 ◽  
Vol 24 (6) ◽  
pp. 865-872 ◽  
Author(s):  
Timothy A. Cudd ◽  
Jeremy S. Wasser ◽  
Wei-Jung A. Chen ◽  
James R. West
Keyword(s):  
31P Nmr ◽  
Alcohol Exposure ◽  
High Energy ◽  
Neonatal Rats ◽  
High Energy Phosphate ◽  
Nmr Study

The effects of hypovolemic hypotension on high-energy phosphate metabolism of traumatized brain in rats

1988 ◽  
Vol 68 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Naoki Ishige ◽  
Lawrence H. Pitts ◽  
Isabelle Berry ◽  
Merry C. Nishimura ◽  
Thomas L. James
Keyword(s):  
High Energy ◽  
High Energy Phosphates ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
Content Type ◽  
Arterial Blood ◽  
High Energy Phosphate Metabolism ◽  
Impact Injury ◽  
Hypovolemic Hypotension

✓ To clarify the effect of hypovolemic hypotension on high-energy phosphate metabolism in head injury, sequential changes in in vivo phosphorus-31 magnetic resonance (31P MR) spectra were compared in 35 rats after impact injury with and without hypotension. Fourteen rats were subjected to hypotension alone (mean arterial blood pressure (MABP) of either 40 or 30 mm Hg for 60 minutes), seven to fluid-percussion impact injury (4 to 5 atm) alone, and 14 to impact injury and hypotension (MABP of 40 to 30 mm Hg). Impact injury alone caused a transient decrease in the phosphocreatine (PCr) level and an increase in the inorganic phosphate (Pi) value. While hypotension alone produced only small changes on 31P MR spectra, impact injury plus hypotension caused pronounced changes. Impact injury and an MABP of 40 mm Hg caused a 50% decrease in PCr concentration and an approximately twofold increase in Pi level, which were significantly greater than values in rats with impact injury alone. Impact injury and an MABP of 30 mm Hg also caused a significant decrease in adenosine triphosphate value, which was not observed in rats with impact injury alone or with an MABP of 30 mm Hg alone. Decreases in intracellular pH were greater in rats with impact injury and hypotension. After traumatic injury, the brain is extremely vulnerable to hypovolemic hypotension, as reflected in the loss of high-energy phosphates in brain.

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