When Does the Lung Die? Time Course of High Energy Phosphate Depletion and Relationship to Lung Viability after "Death"

1995 ◽  
Vol 59 (4) ◽  
pp. 468-474 ◽  
Author(s):  
Andrea M. D'Armini ◽  
Eugene J. Tom ◽  
Charles S. Roberts ◽  
David C. Henke ◽  
John J. Lemasters ◽  
...  
Keyword(s):  
Time Course ◽  
High Energy ◽  
High Energy Phosphate ◽  
Phosphate Depletion

High energy phosphate depletion in leaflet matrix cells during processing of cryopreserved cardiac valves

1992 ◽  
Vol 52 (5) ◽  
pp. 483-488 ◽  
Author(s):  
Robert H. Messier ◽  
Patrick W. Domkowski ◽  
Hamdy M. Aly ◽  
Anwar S. Abd-Elfattah ◽  
Donald G. Crescenzo ◽  
...  
Keyword(s):  
High Energy ◽  
High Energy Phosphate ◽  
Cardiac Valves ◽  
Phosphate Depletion

scholarly journals A temporal dissociation of energy liberation and high energy phosphate splitting during shortening in frog skeletal muscles.

1976 ◽  
Vol 68 (1) ◽  
pp. 13-27 ◽  
Author(s):  
J A Rall ◽  
E Homsher ◽  
A Wallner ◽  
W F Mommaerts
Keyword(s):  
Stimulus Pattern ◽  
Skeletal Muscles ◽  
Energy Production ◽  
Time Course ◽  
Rana Pipiens ◽  
High Energy ◽  
Energy Liberation ◽  
High Energy Phosphate ◽  
Contracting Muscle ◽  
Mechanical Measurements

Measurements of the time course of high energy phosphate splitting and energy liberation were performed on rapidly shortening Rana pipiens skeletal muscles. In muscles contracting 30 times against small loads (less the 0.02P), the ratio of explained heat + work (H + W) (calculated from the measured high energy phosphate splitting) to observed H + W (from myothermal and mechanical measurements) was 0.68 +/- 0.08 and is in agreement with results obtained in isometric tetani of R. pipiens skeletal muscle. In lightly afterloaded muscles which were tetanized for 0.6a and whose metabolism was arrested at 3.0 s after the beginning of stimulation, a similar ratio of explained H + W to observed H + W was obtained. However, in identical contractions in which metabolism was arrested at 0.5-0.75 s after the beginning of stimulation, the ratio of explained H + W to observed H + W declined significantly to values ranging from 0.15 to 0.40. These results suggest that rapid shortening at the beginning of contraction induces a delay between energy production and measurable high energy phosphate splitting. This interpretation was tested and confirmed in experiments in which one muscle of a pair contracted isometrically while the other contracted against a small afterload. The afterload and stimulus pattern were arranged so that at the time metabolism was arrested, 0.5 s after the beginning of stimulation, the total energy production by both muscles was the same. Chemical analysis revealed that the isotonically contracting muscle spilt only 25% as much high energy phosphate as did the isometrically contracting muscle.

Mechanism of the inhibition of myocardial protein synthesis during oxygen deprivation

1976 ◽  
Vol 230 (1) ◽  
pp. 120-126 ◽  
Author(s):  
M Lesch ◽  
H Taegtmeyer ◽  
MB Peterson ◽  
R Vernick
Keyword(s):  
Protein Synthesis ◽  
Metabolic Regulation ◽  
Metabolic Flux ◽  
Adenine Nucleotide ◽  
Krebs Cycle ◽  
High Energy ◽  
Metabolic Inhibitors ◽  
High Energy Phosphate ◽  
Inhibition Of Protein Synthesis ◽  
Phosphate Depletion

Inhibition of protein synthesis during anoxia in the isolated rabbit right ventricular papillary muscle preparation is totally reversible for up to 2 h if glucose concentration is increased during anoxia. The degree of inhibition of protein synthesis during anoxia is, however, not altered by the presence of increased glucose. Thus inhibition of myocardial protein synthesis induced by anoxia need not be related to irreversible disruption of cellular integrity but may represent metabolic regulation of the synthesis. Tissue content of ATP, ADP, AMP, CP, and lactate and phenylalanine incorporation into protein were measured in individual papillary muscles incubated with varying degrees of O2 deprivation and varying substrates and metabolic inhibitors to determine if the inhibition during anoxia could be ascribed to alterations in tissue high-energy phosphate, adenine nucleotide levels, or rate of metabolic flux through the glycolytic and/or Krebs cycle. Protein synthesis was inhibited in muscles incubated in 15 mM glucose during anoxia despite the fact that in the presence of increased glucose, tissue levels of ATP, ADP, and AMP were equal to that of controls. Protein synthesis was normal in muscles made sufficiently hypoxic so that ATP and CP were significantly decreased and lactate increased. Inhibition of Krebs cycle activity with pentenoate failed to effect the rate of protein synthesis. We conclude that anoxic inhibition of myocardial protein synthesis is due neither to high-energy phosphate depletion nor inhibition of Krebs cycle acitivity. The possibility remains that the inhibition may be related to accumulation of glycolytic intermediates or by-products other than lactate.

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