Oxidative and Phosphorylative Metabolism of Rat Liver Tissue Following in Situ Anoxia

1957 ◽  
Vol 191 (1) ◽  
pp. 81-86 ◽  
Author(s):  
John P. Hannon ◽  
S. F. Cook ◽  
Henry A. Leon
Keyword(s):  
Rat Liver ◽  
Liver Tissue ◽  
High Energy ◽  
Morphologic Change ◽  
High Energy Phosphate ◽  
Mitochondrial Oxidation

Rat liver tissue subjected to varying periods of in situ anoxia was investigated in the Warburg apparatus using slices, homogenates and mitochondrial suspensions. Alterations occurring in the respiration of slices were determined by the use of lactate, acetate, citrate and glutamates as well as glucose. Using citrate as a substrate, it was found that homogenate media which contained ATP, when used for slices, prevented the decline in qO2 caused by anoxia. Mitochondrial recovery by the method used here showed a decrease as the anoxia interval progressed. This was found to be caused by a morphologic change attributable to the lack of oxygen. Mitochondrial oxidation and phosphorylation were studied and it was found that in those mitochondria recovered, the ability to produce high-energy phosphate bonds is significantly depressed by anoxia, reaching negligible values within 90 minutes.

High-Energy Phosphate Content of Liver Tissue in Experimental Hemorrhagic Shock

1956 ◽  
Vol 188 (1) ◽  
pp. 86-90 ◽  
Author(s):  
Dorothy K. Rosenbaum ◽  
Edward D. Frank ◽  
Alexander M. Rutenburg ◽  
Howard A. Frank
Keyword(s):  
Hemorrhagic Shock ◽  
Liver Tissue ◽  
Protective Action ◽  
High Energy ◽  
Prior Treatment ◽  
Phosphate Content ◽  
High Energy Phosphate ◽  
Transfusion Therapy ◽  
Energy Stores ◽  
Experimental Hemorrhagic Shock

The ‘high-energy phosphate’ content of liver tissue declines during the course of hemorrhagic shock in the dog. The degree of decline does not correlate with the loss of responsiveness to transfusion therapy. Phosphate energy stores depleted during hemorrhagic shock are rapidly rebuilt following replacement transfusion. Prior treatment with aureomycin reduces the depletion of phosphate energy stores during hemorrhagic shock. Aureomycin given in the same manner has been found to preserve the dog's responsiveness to transfusion therapy. The protective action of aureomycin in hemorrhagic shock is not attributable to the preservation of phosphate energy stores, however, because the change in these stores does not correlate with responsiveness to blood replacement.

High-energy phosphate compounds of rat diaphragm and skeletal muscle fibers

1961 ◽  
Vol 200 (1) ◽  
pp. 182-186 ◽  
Author(s):  
Ruth D. Peterson ◽  
Clarissa H. Beatty ◽  
Rose M. Bocek
Keyword(s):  
Uric Acid ◽  
Absorption Maximum ◽  
Room Temperature ◽  
Creatine Phosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Rat Diaphragm ◽  
High Energy Phosphate ◽  
Atp Levels

The metabolism of high-energy phosphates in a muscle fiber preparation and diaphragm has been investigated. During dissection the creatine phosphate (CrP) level of fibers decreased but was reconstituted during soaking to 61% of the in situ value and remained uncharged during incubation. Dissection and soaking did not affect the adenosinetriphosphate + adenosinediphosphate (ATP + ADP) levels but incubation caused small decreases. Similar decreases in CrP and ATP levels of diaphragm occurred during incubation. The decreases in the ATP levels in fibers and diaphragm correlated with decreases in adenine absorption. A concomitant shift occurred in the absorption peak of fiber media toward the absorption maximum of hypoxanthine. In contrast, the curves for diaphragm media showed a progressive shift toward the absorption maximum for uric acid. Uricase analyses demonstrated uric acid in diaphragm media. The mesothelial covering of the diaphragm was shown to have a separate and distinct metabolism which converts hypoxanthine to uric acid. Soaking the fibers in iced buffer instead of buffer at room temperature decreased the CrP levels after incubation, ATP values were unaffected.

In situ rat fast skeletal muscle is more efficient at submaximal than at maximal activation levels

2002 ◽  
Vol 92 (5) ◽  
pp. 2089-2096 ◽  
Author(s):  
F. Abbate ◽  
C. J. De Ruiter ◽  
C. Offringa ◽  
A. J. Sargeant ◽  
A. De Haan
Keyword(s):  
Gastrocnemius Muscle ◽  
Chemical Change ◽  
High Energy ◽  
Medial Gastrocnemius ◽  
High Energy Phosphate ◽  
Energy Turnover ◽  
Maximal Activation ◽  
Low Efficiency ◽  
Medial Gastrocnemius Muscle

The influence of stimulation frequency on efficiency (= total work output/high-energy phosphate consumption) was studied using in situ medial gastrocnemius muscle tendon complexes of the rat. The muscles performed 20 repeated concentric contractions (2/s) at 34°C. During these repeated contractions, the muscle was stimulated via the severed sciatic nerve with either 60, 90, or 150 Hz. The muscle was freeze-clamped immediately after these contractions, and high-energy phosphate consumption was determined by measuring intramuscular chemical change relative to control muscles. The average values (±SD) of efficiency calculated for 60, 90, and 150 Hz were 18.5 ± 1.5 ( n = 7), 18.6 ± 1.5 ( n = 9), and 14.7 ± 1.3 mJ/μmol phosphate ( n = 9). The results indicate that the efficiency of the muscles that were submaximally activated (60 or 90 Hz) was higher (+26%, P < 0.05) than that of those maximally activated (150 Hz). Additional experiments showed that the low efficiency at maximal activation levels is unlikely to be the result of a higher energy turnover by the Ca2+-ATPase relative to the total energy turnover. Therefore, alternative explanations are discussed.

Phosphorylated beta-guanidinopropionate as a substitute for phosphocreatine in rat muscle

1975 ◽  
Vol 228 (4) ◽  
pp. 1123-1125 ◽  
Author(s):  
CD Fitch ◽  
M Jellinek ◽  
RH Fitts ◽  
KM Baldwin ◽  
JO Holloszy
Keyword(s):  
Muscle Contraction ◽  
Tibialis Anterior ◽  
High Energy ◽  
High Energy Phosphate ◽  
Tension Development ◽  
Rat Muscle ◽  
Peak Value

To evaluate phosphorylated beta-guanidinopropionate (beta-GPAP) as a substitute for phosphocreatine (PC), hypoxic tibialis anterior muscles were stimulated to contract isometrically in situ until twitch tension fell to 25 percent of the peak value. Muscles from rats fed beta-guanidinopropionic acid (beta-GPA) failed to exhibit the staircase phenomenon, and they developed 28 percent less tension than control muscles. In control muscles lactate increased from 0.75 to 20.99, ADP increased from 0.89 to 1.20, ATP decreased from 5.09 to 2.73, and PC decreased from 15.78 to 1.52 mumol/g. In muscles from rats fed beta-GPA, lactate increased from 0.85 to 14.31, ADP increased from 0.86 to 1.05, ATP decreased from 2.69 to 1.71, PC decreased from 0.73 to 0.30, and beta-GPAP decreased from 30.34 to 19.45 mumol/g. From these measurements, the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate and tension development confirm experimentally the ability of beta-GPAP to substitute for PC as a source of energy to sustain muscle contraction.

Cerebral oxidative metabolism and redox state during hypoxia-ischemia and early recovery in immature rats

1991 ◽  
Vol 261 (4) ◽  
pp. H1102-H1108
Author(s):  
J. Y. Yager ◽  
R. M. Brucklacher ◽  
R. C. Vannucci
Keyword(s):  
Carotid Artery ◽  
Tricarboxylic Acid Cycle ◽  
Recovery Period ◽  
High Energy ◽  
Artery Occlusion ◽  
High Energy Phosphate ◽  
Early Recovery ◽  
Artery Ligation ◽  
Hypoxia Ischemia ◽  
Mitochondrial Oxidation

Intracellular pH (pHi) and cytoplasmic and mitochondrial oxidation-reduction (redox) states of cerebral tissue were examined in relation to perturbations of glycolytic and tricarboxylic acid cycle intermediates and of high-energy phosphate reserves during hypoxia-ischemia and the early recovery period in the immature rat. Seven-day postnatal rats underwent unilateral common carotid artery ligation and exposure to 8% O2 for 3 h, after which they were quick frozen in liquid N2 at the terminus of hypoxia-ischemia and at 10, 30, 60, and 240 min of recovery for enzymatic fluorometric analysis of cerebral metabolites. During hypoxia-ischemia, concentrations of glucose and alpha-ketoglutarate in the cerebral hemisphere ipsilateral to the carotid artery occlusion were depleted to 10 and 70% of control, respectively; pyruvate was unchanged. During recovery, glucose, pyruvate, and alpha-ketoglutarate increased above their respective control values. Calculated pHi decreased from 7.0 (control) to 6.6 during hypoxia-ischemia and normalized by 10 min of recovery. The cytoplasmic NAD+/NADH ratio decreased (increased reduction) to 50% of control during hypoxia-ischemia and remained in the reduced state throughout 4 h of recovery. Paradoxically, mitochondrial NAD+/NADH was oxidized at the terminus of hypoxia-ischemia. The mitochondrial oxidation which developed during hypoxia-ischemia presumably results from a limitation of cellular substrate (glucose) supply, which in turn leads to a depletion of high-energy phosphate reserves, culminating in brain damage.

Initial Polymerization Sites Indicated During Mitochondrial Oxidation of Diaminobenzidine after Toluene Treatment

1977 ◽  
Vol 35 ◽  
pp. 408-409
Author(s):  
W. A. Shannon ◽  
M. A. Matlib
Keyword(s):  
Membrane Permeability ◽  
Cytochrome Oxidase ◽  
Rat Liver ◽  
Precise Definition ◽  
Cytochemical Localization ◽  
Oxidative Reaction ◽  
Mitochondrial Oxidation ◽  
Definition Of ◽  
Exogenous Substrates

Numerous studies have dealt with the cytochemical localization of cytochrome oxidase via cytochrome c. More recent studies have dealt with indicating initial foci of this reaction by altering incubation pH (1) or postosmication procedure (2,3). The following study is an attempt to locate such foci by altering membrane permeability. It is thought that such alterations within the limits of maintaining morphological integrity of the membranes will ease the entry of exogenous substrates resulting in a much quicker oxidation and subsequently a more precise definition of the oxidative reaction.The diaminobenzidine (DAB) method of Seligman et al. (4) was used. Minced pieces of rat liver were incubated for 1 hr following toluene treatment (5,6). Experimental variations consisted of incubating fixed or unfixed tissues treated with toluene and unfixed tissues treated with toluene and subsequently fixed.

In situ TEM studies of irradiation effects for materials improvement

1991 ◽  
Vol 49 ◽  
pp. 452-453
Author(s):  
Charles W. Allen
Keyword(s):  
Nuclear Reactor ◽  
Austenitic Stainless Steels ◽  
High Energy ◽  
Point Of View ◽  
In Situ Tem ◽  
Irradiation Effects ◽  
Tem Analysis ◽  
Radiation Induced ◽  
Analytical Tools

Irradiation effects studies employing TEMs as analytical tools have been conducted for almost as many years as materials people have done TEM, motivated largely by materials needs for nuclear reactor development. Such studies have focussed on the behavior both of nuclear fuels and of materials for other reactor components which are subjected to radiation-induced degradation. Especially in the 1950s and 60s, post-irradiation TEM analysis may have been coupled to in situ (in reactor or in pile) experiments (e.g., irradiation-induced creep experiments of austenitic stainless steels). Although necessary from a technological point of view, such experiments are difficult to instrument (measure strain dynamically, e.g.) and control (temperature, e.g.) and require months or even years to perform in a nuclear reactor or in a spallation neutron source. Consequently, methods were sought for simulation of neutroninduced radiation damage of materials, the simulations employing other forms of radiation; in the case of metals and alloys, high energy electrons and high energy ions.

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