scholarly journals Some factors affecting phosphate transport in a perfused rat heart preparation

1980 ◽  
Vol 188 (2) ◽  
pp. 297-311 ◽  
Author(s):  
G Medina ◽  
J Illingworth
Keyword(s):  
Rat Heart ◽  
Prolonged Exposure ◽  
Work Load ◽  
Phosphate Transport ◽  
Aortic Pressure ◽  
Efflux Rate ◽  
Cardiac Work ◽  
Factors Affecting ◽  
Perfused Rat Heart ◽  
Heart Preparation

Pi uptake by a perfused rat heart preparation did not require the presence of any other permeant anion, but was markedly dependent on the extracellular Na+ concentration and accelerated when tissue oxygenation was inadequate. Pi efflux was also independent of other permeant anions, but apparently varied with the intracellular Na+ concentration. Cardiac Pi efflux was not sensitive to a number of inhibitors that clock Cl- movement in heart and other tissues. Both uptake and efflux apparently proceed via a reversible electroneutral co-transport system linked to the transmembrane Na+ gradient. Pi uptake was independent of cardiac work load, but the efflux rate was sharply accelerated after an increase in aortic pressure development, with a slow return towards basal values during sustained periods of high work output. An inverted biphasic effect on the efflux rate was observed after a reduction in cardiac work load. Mild hypoxia and respiratory and metabolic acidosis each resulted in a transient acceleration of Pi efflux followed by a return towards basal values during prolonged exposure to the stimulus, whereas respiratory and metabolic alkalosis produced a similar but inverted response. The origin of these phasic effects on Pi efflux remains to be identified at present.

scholarly journals Effects of pressure overload and insulin on protein turnover in the perfused rat heart. Prostaglandins are not involved although their synthesis is stimulated by insulin

1987 ◽  
Vol 243 (2) ◽  
pp. 473-479 ◽  
Author(s):  
D M Smith ◽  
P H Sugden
Keyword(s):  
Protein Synthesis ◽  
Protein Turnover ◽  
Rat Heart ◽  
Pressure Overload ◽  
Aortic Pressure ◽  
Prostaglandin Synthesis ◽  
Perfused Rat Heart ◽  
Heart Preparation ◽  
Synthesis And Degradation

A modified anterogradely perfused rat heart preparation is described in which all the cardiac output passes through the coronary circulation. Such a preparation develops hypertensive aortic pressures. Hypertensive aortic pressures or insulin stimulate the rate of cardiac protein synthesis and inhibit the rate of protein degradation. Aortic pressure and insulin may be important in the regulation of cardiac nitrogen balance in vivo. By abolishing cardiac prostaglandin synthesis with 4-biphenylacetate, we were able to investigate the possible involvement of prostaglandins in the modulation of protein turnover by pressure overload or insulin. There was no evidence of any involvement. However, insulin stimulated and cycloheximide inhibited cardiac prostaglandin synthesis. These findings are consonant with an enzyme involved in prostaglandin synthesis being short-lived and prostaglandin synthesis being rapidly influenced by activators and inhibitors of protein synthesis and degradation.

Computer simulation of metabolism of glucose-perfused rat heart in a work-jump

1982 ◽  
Vol 243 (3) ◽  
pp. R389-R399
Author(s):  
M. J. Achs ◽  
D. Garfinkel ◽  
L. H. Opie
Keyword(s):  
Rat Heart ◽  
Tricarboxylic Acid Cycle ◽  
Lactate Production ◽  
Work Load ◽  
Creatine Phosphate ◽  
Glycolytic Intermediate ◽  
Rapid Fall ◽  
Heart Preparation ◽  
Early Rise

A computer model of glycolysis, the tricarboxylic acid cycle, and related amino acid metabolism, is described for a glucose-perfused experimental rat heart preparation suddenly switched from low work load (Langendorff perfusion) to high work load (left atrial perfusion). Glycolytic intermediate measurements suggest activation of phosphofructokinase within a few seconds. This activation, and also that of other glycolytic enzymes, is calculated as due to a sharp increase in cytoplasmic Mg2+ level, which overcomes the inhibitory effects of a rapid fall in cytoplasmic pH to 6.77 (calculated from a rapid fall in creatine phosphate). Increased glycolytic substrate is initially supplied by glycogenolysis mediated by phosphorylase b (activated by an early rise in cytoplasmic AMP), followed by increased glucose uptake from the perfusate. Testable predictions are made by the model, especially that lactate production rate should peak early. Additional experiments are described that verify these predictions and fill gaps in the original measurements. The role of modeling in interpreting such experiments is discussed.

Differential effects of cysteine on protein and coenzyme A synthesis in rat heart

1984 ◽  
Vol 247 (1) ◽  
pp. C99-C106 ◽  
Author(s):  
B. H. Chua ◽  
K. E. Giger ◽  
B. J. Kleinhans ◽  
J. D. Robishaw ◽  
H. E. Morgan
Keyword(s):  
Protein Synthesis ◽  
Rat Heart ◽  
Coenzyme A ◽  
Pantothenic Acid ◽  
Fold Increase ◽  
Creatine Phosphate ◽  
Aortic Pressure ◽  
Protective Agent ◽  
Bicarbonate Buffer ◽  
Perfused Rat Heart

The effect of cysteine availability on protein and coenzyme A (CoA) synthesis in perfused rat heart was incompletely evaluated in earlier experiments because rapid conversion of cysteine to cystine occurred when the perfusion buffer was oxygenated. This conversion was minimized by addition of an excess of reducing agents such as dithiothreitol or mercaptodextran or by provision of bathocuproine disulfonate, a copper chelator. Dithiothreitol was not a suitable protective agent because it reduced ATP and creatine phosphate contents. Perfusion of hearts with [35S]cystine or [35S]cysteine in the presence of mercaptodextran resulted in a 22-fold or 5-fold increase, respectively, in incorporation of [35S] into protein and a 5-fold or 8-fold increase, respectively, in incorporation into CoA compared with hearts supplied [35S]cystine or [35S]cysteine without the reducing agent. When compared with hearts perfused at an aortic pressure of 90 mmHg with bicarbonate buffer that contained 15 mM glucose, 25 mU insulin/ml, 0.4 mM [14C]phenylalanine, no cysteine and plasma levels of other amino acids, provision of 0.09 or 0.2 mM cysteine alone or in the presence of mercaptodextran, or bathocuproine disulfonate enhanced rates of protein synthesis 16-35%. When 0.2 mM cysteine was added to bicarbonate buffer containing 7 microM pantothenic acid, supplementation with mercaptodextran or bathocuproine disulfonate was required to raise CoA content. These results indicated that an exogenous supply of cysteine was needed to maintain maximal rates of protein and CoA synthesis in the perfused rat heart. Protective compounds were required to obtain the cysteine effect on CoA but not on protein synthesis.

The Isolated Perfused Heart and Its Pioneers

Physiology ◽  
1998 ◽  
Vol 13 (4) ◽  
pp. 203-210 ◽  
Author(s):  
Heinz-Gerd Zimmer
Keyword(s):  
Rat Heart ◽  
Frog Heart ◽  
Isolated Perfused Heart ◽  
Perfused Heart ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Mammalian Heart ◽  
Heart Preparation ◽  
The 1960S

In 1866, Carl Ludwig together with Elias Cyon created the first isolated perfused frog heart preparation. Perfusion systems for the isolated mammalian heart were developed by H. Newell Martin in 1883 and by Oscar Langendorff in 1895. In its working mode, the isolated perfused rat heart was established in the 1960s.

Computer simulation of metabolism in pyruvate-perfused rat heart. II. Krebs cycle

1979 ◽  
Vol 237 (3) ◽  
pp. R159-R166 ◽  
Author(s):  
M. C. Kohn ◽  
M. J. Achs ◽  
D. Garfinkel
Keyword(s):  
Redox Potential ◽  
Rat Heart ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Krebs Cycle ◽  
Coordinated Control ◽  
Work Load ◽  
Metabolic Model ◽  
Tricarboxylic Acid ◽  
Perfused Rat Heart

A realistic metabolic model of the tricarboxylic acid cycle in the perfused rat heart was constructed to help explain the sequence of biochemical events regulating the metabolism of exogenous pyruvate following a large increase in work load. The unchelated Mg2+ level was the most important controlling factor. The resulting mixture of chelated and unchelated nucleotides and tribasic acids effected coordinated control of citrate synthase, aconitase, isocitrate dehydrogenase, succinyl CoA synthetase, fumarase, and nucleoside diphosphokinase, because Mg2+-chelates are generally substrates whereas unchelated species are inhibitors. Succinate dehydrogenase is largely controlled by the ubiquinone redox potential. The fluxes through alpha-ketoglutarate and malate dehydrogenases are largely dependent on thepyridine nucleotide redox potential, but the succinyl CoA-to-CoASH ratio strongly affects the former enzyme as well. The model predicts an accumulation of succinate during the transition to higher work output.

Computer simulation of metabolism in pyruvate-perfused rat heart. V. Physiological implications

1979 ◽  
Vol 237 (3) ◽  
pp. R181-R186 ◽  
Author(s):  
D. Garfinkel ◽  
M. C. Kohn ◽  
M. J. Achs
Keyword(s):  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Work Load ◽  
Physiological Signals ◽  
Sudden Increase ◽  
Energy Reserves ◽  
Phosphate Potential ◽  
Atp Level ◽  
Perfused Rat Heart ◽  
Weakly Coupled

The results of a simulation of metabolism in the pyruvate-perfused rat heart subjected to a sudden increase in work load are interpreted to provide a coherent explanation for the observed physiology. Respiration is most closely correlated with the mitochondrial phosphate potential, calculated from the MgATP and MgADP levels. No correlation between respiration and the pH gradient across the mitochondrial membrane was found. The transient falls in pH in the cytosol and perhaps the mitochondria are due largely to carbonic and lactic acidosis and appear to be only weakly coupled. The heart maintains a high ATP level during the transition to increased work by utilizing its energy reserves in order of decreasing availability in response to physiological signals mediated by Mg2+, Ca2+, and cAMP.

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