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.

NMR study of rat diaphragm exposed to metabolic and compensated metabolic acidosis

1988 ◽  
Vol 65 (5) ◽  
pp. 2278-2284 ◽  
Author(s):  
R. S. Fitzgerald ◽  
S. Howell ◽  
M. M. Pike ◽  
W. E. Jacobus
Keyword(s):  
Metabolic Acidosis ◽  
31P Nmr ◽  
Mechanical Performance ◽  
High Energy ◽  
31P Nmr Spectroscopy ◽  
Rat Diaphragm ◽  
Cardiac Sarcolemma ◽  
Sample Tube ◽  
Nmr Study ◽  
Residual Capacity

When exposed to hypercapnia, several muscles deteriorate with respect to their mechanical performance. Exposure to metabolic acidosis and, perhaps surprisingly, to compensated metabolic acidosis has the same effect on the diaphragm. The mechanisms involved in these effects remain unclear. If the diaphragmatic intracellular pH (pHi) is assumed to decrease with hypercapnia, to remain unchanged during metabolic acidosis, and to increase during compensated metabolic acidosis, it would appear that different mechanisms must be responsible for the depreciation in the diaphragm's mechanical performance. The present experiments using 31P nuclear magnetic resonance (31P-NMR) spectroscopy were undertaken to determine the effect of metabolic acidosis and compensated metabolic acidosis on pHi and on high-energy phosphate metabolites in the resting rat diaphragm. A whole diaphragm was slightly stretched while being stitched onto a fiberglass mesh. The area approximated that at functional residual capacity. It was superfused in the NMR sample tube with a phosphate-free Krebs-Ringer bicarbonate solution [( HCO3-] = 6 meqO equilibrated with either 95% O2-5% CO2 or 98.75% O2-1.25% CO2). Spectra were acquired during 15-min intervals for control (30 min of normal Krebs-Ringer bicarbonate superfusate, equilibrated with 95% O2-5% CO2), for 120 min of exposure to either form of acidosis and for 60 min of recovery with normal superfusate. The pHi decreased rapidly during metabolic acidosis but did not change significantly during compensated metabolic acidosis. In both forms of acidosis, phosphocreatine declined gradually but not significantly, whereas ATP and inorganic phosphate did not change at all. The results suggest that HCO3- passes freely through the diaphragmatic sarcolemma, very much like the cardiac sarcolemma.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of input pressure on in vitro turtle heart during anoxia and acidosis: a 31P-NMR study

1995 ◽  
Vol 268 (3) ◽  
pp. R683-R689 ◽  
Author(s):  
D. C. Jackson ◽  
H. Shi ◽  
J. H. Singer ◽  
P. H. Hamm ◽  
R. G. Lawler
Keyword(s):  
31P Nmr ◽  
Mechanical Performance ◽  
Creatine Phosphate ◽  
31P Nmr Spectroscopy ◽  
Nmr Study ◽  
Input Pressure ◽  
In Series ◽  
Series Of Experiments ◽  
Phosphorus Metabolites

In vitro working hearts of the turtle, Chrysemys picta bellii, paced at 30 beats/min, were studied over a range of input pressures in the following sequence of perfusion conditions: control normoxia, control anoxia, lactacidotic normoxia, and lactacidotic anoxia. Two such series of experiments were performed. In series 1 (n = 12), ventricular pressure (PV) and cardiac output were measured, and power output and dPV/dt were calculated. In series 2 (n = 5), intracellular phosphorus metabolites and intracellular pH (pHi) were also measured using 31P-nuclear magnetic resonance (31P-NMR) spectroscopy. In series 1 all mechanical variables increased with input pressure in generally similar fashion, except during anoxic acidosis, during which mechanical performance was depressed and was increased less or not at all by input pressure. Creatine phosphate (CP) and pHi fell significantly in anoxia and anoxic acidosis, but neither these variables, ATP, CP/ATP, nor, presumably, ADP changed as a function of input pressure with any perfusate despite often large increments in mechanical output. We conclude that anoxia and acidosis act synergistically to depress cardiac function in turtle hearts. Also, the insensitivity of NMR variables to changes in input pressure and cardiodynamics suggests that changes in these variables are unimportant for controlling energy turnover in this preparation.

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

An in vivo examination of rat brain during sepsis with 31P-NMR spectroscopy

1989 ◽  
Vol 257 (6) ◽  
pp. C1055-C1061 ◽  
Author(s):  
R. S. Hotchkiss ◽  
R. C. Long ◽  
J. R. Hall ◽  
G. T. Shires ◽  
R. G. Brouillard ◽  
...  
Keyword(s):  
Time Course ◽  
31P Nmr ◽  
Severe Infection ◽  
High Energy ◽  
Control Group ◽  
31P Nmr Spectroscopy ◽  
High Energy Phosphates ◽  
Arterial Blood ◽  
Brain Ph

Neurological symptoms including lethargy, obtundation, and confusion are early and common findings in patients with sepsis. The etiology of the mental status changes that occur during severe infection is not known. We investigated the effects of sepsis on the levels of high-energy phosphates to determine whether decreased energy metabolism was a factor in the depressed neurological state. The time course of changes in brain pH and brain high-energy phosphate metabolites during an Escherichia coli infusion was determined from sequential phosphorus-31 nuclear magnetic resonance (31P-NMR) spectra of ketamine-xylazine-anesthetized rats. A second group of rats received 0.9% saline infusion and served as a control group. Despite severe obtundation and near loss of righting reflex, the rats in the septic group had no significant differences in the brain pH, the ratio of phosphocreatine (PCr) to beta-adenosine 5'-triphosphate (beta-ATP), or in the ratio of PCr to Pi. The only significant decrease in brain high-energy phosphates or pH occurred terminally in the septic rat group and corresponded with a rapidly falling arterial blood pressure. We conclude that the severe neurological depression that is characteristic of sepsis is not due to decreased levels of brain high-energy phosphates or brain acidosis.

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

scholarly journals In vivo and in vitro 31P-NMR Study of the Phosphate Transport and Polyphosphate Metabolism in Hebeloma cylindrosporum in Response to Plant Roots Signals

BIO-PROTOCOL ◽  
2018 ◽  
Vol 8 (16) ◽  
Author(s):  
Christine Le Guerneve ◽  
Adeline Becquer ◽  
Margarita Torres-Aquino ◽  
Laurie Amenc ◽  
Carlos Trives-Segura ◽  
...  
Keyword(s):  
31P Nmr ◽  
Phosphate Transport ◽  
Plant Roots ◽  
Hebeloma Cylindrosporum ◽  
Nmr Study ◽  
Polyphosphate Metabolism

Skeletal muscle bioenergetics during frequency-dependent fatigue

1991 ◽  
Vol 260 (3) ◽  
pp. C643-C651 ◽  
Author(s):  
C. R. Bridges ◽  
B. J. Clark ◽  
R. L. Hammond ◽  
L. W. Stephenson
Keyword(s):  
Skeletal Muscle ◽  
Nmr Spectroscopy ◽  
31P Nmr ◽  
High Energy ◽  
Metabolic Energy ◽  
31P Nmr Spectroscopy ◽  
External Work ◽  
Dynamic Contractions ◽  
High Energy Phosphate Metabolism

The bioenergetic correlates of skeletal muscle fatigue were assessed in vivo with phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy. After surgical construction of latissimus dorsi muscle ventricles, seven beagles underwent 31P-NMR spectroscopy during 12-min exercise protocols at 25- and 85-Hz stimulation frequencies and during both isovolumetric and dynamic contractions. Exercise at 85 Hz was associated with significantly greater fatigue than exercise at 25 Hz. At both frequencies, the onset of exercise was associated with a marked increase in inorganic phosphate (Pi) and a decrease in phosphocreatine (PCr). As the muscle fatigued at 85 Hz but not at 25 Hz, the phosphorus spectra returned to near baseline with a decrease in Pi and increase in PCr. For a given amount of force generated, the Pi-to-PCr ratio was higher for dynamic contractions than for isovolumetric contractions. This study indicates that high-frequency fatigue is unlikely to result from the direct effects of high-energy phosphate metabolism and that contractions producing external work consume more metabolic energy than equally forceful isometric contractions.

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.

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