scholarly journals The effect of prolonged anoxia at 3°C on tissue high energy phosphates and phosphodiesters in turtles: A 31P-NMR study

1995 ◽  
Vol 165 (1) ◽  
pp. 77-84 ◽  
Author(s):  
D. C. Jackson ◽  
S. J. Warburton ◽  
E. Arendt Meinertz ◽  
R. G. Lawler ◽  
J. S. Wasser
Keyword(s):  
31P Nmr ◽  
High Energy ◽  
High Energy Phosphates ◽  
Nmr Study

Activation of dehydrogenase activity and cardiac respiration: a 31P-NMR study

1988 ◽  
Vol 255 (1) ◽  
pp. H185-H188 ◽  
Author(s):  
L. A. Katz ◽  
A. P. Koretsky ◽  
R. S. Balaban
Keyword(s):  
Oxygen Consumption ◽  
Pyruvate Dehydrogenase ◽  
31P Nmr ◽  
High Energy ◽  
Ruthenium Red ◽  
High Energy Phosphates ◽  
Perfused Heart ◽  
Nmr Studies ◽  
Heart Work ◽  
Nmr Study

31P-NMR studies were performed to determine the tissue phosphate and oxygen consumption effects of known maneuvers on the activation of pyruvate dehydrogenase during work jumps in the perfused rat heart. In control studies of the glucose-perfused heart, work jumps, with pacing, resulted in a 32% increase in oxygen consumption (QO2) from 1.72 +/- 0.09 to 2.29 +/- 0.12 mmol O2.h-1.g dry wt-1. During this transition no significant change in the high energy phosphates were detected. In contrast, work jumps did cause changes in the phosphates when the activation of pyruvate dehydrogenase was blocked with 2.5 micrograms of ruthenium red per milliliter or maximally stimulated with 11 mM pyruvate before the increase in work. The observed increase in QO2 and inorganic phosphate and calculated increase in ADP are consistent with these phosphates controlling mitochondrial respiration under these conditions. These results suggest that the activation of pyruvate dehydrogenase and/or other dehydrogenases may be an important step in the orchestration of work and QO2.

Sustained function of normoxic hearts depleted in ATP and phosphocreatine: a 31P-NMR study

1988 ◽  
Vol 255 (2) ◽  
pp. C192-C201 ◽  
Author(s):  
J. A. Hoerter ◽  
C. Lauer ◽  
G. Vassort ◽  
M. Gueron
Keyword(s):  
31P Nmr ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
High Energy ◽  
High Energy Phosphates ◽  
Drastic Reduction ◽  
Nmr Study ◽  
Unit Work ◽  
Phosphate Depletion

A model of high-energy phosphate depletion was developed in the normoxic isovolumic rat heart perfused with acetate, 2-deoxy-D-glucose (2DG), and insulin. Intracellular phosphorylation of 2DG abstracts phosphorus from its normal pathways. This results in a decrease of high-energy phosphates without any increase in Pi. During the first 15 min of 2DG phosphorylation, the changes in ATP, Pi, and intracellular pH (pHi) were slight, and work was unaltered, although phosphocreatine (PCr) concentration dropped by 50%. After 45 min, the heart reached a new steady state characterized by a drastic reduction in both PCr and ATP: PCr was 15% of control, and in most hearts ATP became invisible on the nuclear magnetic resonance (NMR) spectra. Nevertheless, the heart still developed 65% of its original systolic pressure, whereas diastolic pressure was unchanged. Oxygen consumption per unit work remained constant during 2DG perfusion. This is, to our knowledge, the first experimental model of sustained cardiac contractility at such low contents of both ATP and PCr. However, our results are compatible with present knowledge of the cytosolic energy transfer by PCr and of the control of force in myofilaments.

31P-NMR study of resting in vitro rat diaphragm exposed to hypercapnia

1988 ◽  
Vol 65 (5) ◽  
pp. 2270-2277 ◽  
Author(s):  
R. S. Fitzgerald ◽  
S. Howell ◽  
W. E. Jacobus
Keyword(s):  
31P Nmr ◽  
Mechanical Performance ◽  
High Energy ◽  
31P Nmr Spectroscopy ◽  
High Energy Phosphates ◽  
Rat Diaphragm ◽  
Nmr Study

We have reported previously that, when exposed to hypercapnia of various intensities, the diaphragm reduces its force of twitch and tetanic contractions in the in vitro rat preparation as well as in the in vivo dog preparation. The experiments reported here with 31P nuclear magnetic resonance (31P-NMR) spectroscopy attempt to examine cellular mechanisms that might be responsible for this deterioration in mechanical performance. Specifically they describe certain characteristics of this preparation and cautions needed to study the resting in vitro rat diaphragm with such techniques. Second, they report the response of intracellular pH (pHi), phosphocreatine (PCr), ATP, and inorganic phosphate (Pi) in the resting in vitro rat diaphragm exposed to long-term normocapnia or to long-term hypercapnia. The results show that 1) to maintain a viable preparation, it was necessary to keep the diaphragm extended to an area approximating that at functional residual capacity, 2) the diaphragm seemed quite capable of maintaining a constant pHi and constant contents of ATP and Pi during normocapnia, but there was a gradual decline in PCr, and 3) during hypercapnia there was a significant decrease in pHi, but the behavior of the phosphate metabolites was exactly as during normocapnia. The results suggest that the decrease in mechanical performance of the diaphragm is probably not due to a decrease in the availability of the high-energy phosphates, although they do not completely exclude this possibility or possibilities related to regional compartmentation.

Depletion of high energy phosphates implicates post-exercise mortality in carp and trout; an in vivo 31P-NMR study

2008 ◽  
Vol 149 (1) ◽  
pp. 98-108 ◽  
Author(s):  
Vincent van Ginneken ◽  
Karen Coldenhoff ◽  
Ron Boot ◽  
Johan Hollander ◽  
Fons Lefeber ◽  
...  
Keyword(s):  
31P Nmr ◽  
High Energy ◽  
High Energy Phosphates ◽  
Post Exercise ◽  
Nmr Study

Reduced substrate oxidation in postischemic myocardium: 13C and 31P NMR analyses

1990 ◽  
Vol 258 (5) ◽  
pp. H1357-H1365 ◽  
Author(s):  
E. D. Lewandowski ◽  
D. L. Johnston
Keyword(s):  
Steady State ◽  
31P Nmr ◽  
Tca Cycle ◽  
High Energy ◽  
Substrate Oxidation ◽  
High Energy Phosphates ◽  
Atp Content ◽  
And Control ◽  
13C And 31P Nmr ◽  
Postischemic Myocardium

13C and 31P nuclear magnetic resonance (NMR) spectra were used to assess substrate oxidation and high-energy phosphates in postischemic (PI) isolated rabbit hearts. Phosphocreatine (PCr) increased in nonischemic controls on switching from glucose perfusion to either 2.5 mM [3-13C]pyruvate (120%, n = 7) or [2-13C]acetate (114%, n = 8, P less than 0.05). ATP content, oxygen consumption (MVO2), and hemodynamics (dP/dt) were not affected by substrate availability in control or PI hearts. dP/dt was 40-60% lower in PI hearts during reperfusion after 10 min ischemia. Hearts reperfused with either pyruvate (n = 11) or acetate (n = 8) regained preischemic PCr levels within 45 s. Steady-state ATP levels were 55-70% of preischemia with pyruvate and 52-60% with acetate. Percent maximum [4-13C]glutamate signal showed reduced conversion of pyruvate to glutamate via the tricarboxylic acid (TCA) cycle at 4-min reperfusion (PI = 24 +/- 4%, means +/- SE; Control = 48 +/- 4%). The increase in 13C signal from the C-4 position of glutamate was similar to control hearts within 10.5 min. The increase in [4-13C]glutamate signal from acetate was not different between PI and control hearts. The ratio of [2-13C]Glu:[4-13C]Glu, reflecting TCA cycle activity, was reduced in PI hearts with acetate for at least 10 min (Control = 0.76 +/- 0.03; PI = 0.51 +/- 0.09) until steady state was reached. Despite rapid recovery of oxidative phosphorylation, contractility remained impaired and substrate oxidation was significantly slowed in postischemic hearts.

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