In vivo phosphorus-31 NMR spectroscopy of abnormal myocardial high-energy phosphate metabolism during cardiac stress in hypertensive-hypertrophied non-human primates

1990 ◽  
Vol 6 (1) ◽  
pp. 57-70 ◽  
Author(s):  
D. Douglas Miller ◽  
Richard A. Walsh
2000 ◽  
Vol 10 (6) ◽  
pp. 610-617 ◽  
Author(s):  
Andrea B. Eidenschink ◽  
Gerrit Schröter ◽  
Stefan Müller-Weihrich ◽  
Heiko Stern

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.


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

2003 ◽  
Vol 76 (5) ◽  
pp. 622-633 ◽  
Author(s):  
David M. Bailey ◽  
Lloyd S. Peck ◽  
Christian Bock ◽  
Hans‐Otto Pörtner

1988 ◽  
Vol 68 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Naoki Ishige ◽  
Lawrence H. Pitts ◽  
Isabelle Berry ◽  
Merry C. Nishimura ◽  
Thomas L. James

✓ 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.


1987 ◽  
Vol 67 (5) ◽  
pp. 649-653 ◽  
Author(s):  
Paul A. Murray ◽  
Thomas J. J. Blanck ◽  
Mark C. Rogers ◽  
William E. Jacobus

1998 ◽  
Vol 95 (2) ◽  
pp. 250-255
Author(s):  
J. F. Toussaint ◽  
C. Brillault-Salvat ◽  
E. Giacomini ◽  
G. Bloch ◽  
D. Duboc ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document