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.

Effect of hypoxia on myocardial high-energy phosphates in the neonatal mammalian heart

1978 ◽  
Vol 235 (5) ◽  
pp. H475-H481 ◽  
Author(s):  
J. M. Jarmakani ◽  
T. Nagatomo ◽  
M. Nakazawa ◽  
G. A. Langer
Keyword(s):  
Lactate Production ◽  
Creatine Phosphate ◽  
High Energy ◽  
Adult Rabbit ◽  
High Energy Phosphates ◽  
Mechanical Function ◽  
High Energy Phosphate ◽  
Buffer Solution ◽  
Bicarbonate Buffer ◽  
Atp Concentration

The effect of hypoxia on myocardial high-energy phosphate content in the newborn, 2-wk-old, and adult rabbit was determined and compared with mechanical function. Studies were done on the ventricular septum arterially perfused with Krebs-Henseleit bicarbonate buffer solution equilibrated with 95% O2 and 5% CO2 (control) or 95% N2 and 5% CO2 (hypoxia) at 60 beats/min and 27 degrees C. In the adult, ATP concentration decreased to 68%, 56%, and 39% of control after 2, 30, and 60 min of hypoxia, respectively. After 30 min of hypoxia, ATP concentration was not different from control in the newborn but decreased to 82% of control in the 2-wk-old. After 2 min of hypoxia, creatine phosphate concentration decreased to 55% and 10% of control in the newborn and adult rabbit, respectively. Lactate production increased significantly during hypoxia and was greater in the newborn than in the adult. The data indicate that the newborn rabbit is capable of maintaining glycolysis and normal levels of myocardial ATP during hypoxia, which ensures normal myocardial mechanical function for longer periods than in the adult.

Superoxide scavengers augment contractile but not energetic responses to hypoxia in rat diaphragm

2005 ◽  
Vol 98 (5) ◽  
pp. 1753-1760 ◽  
Author(s):  
V. P. Wright ◽  
P. F. Klawitter ◽  
D. F. Iscru ◽  
A. J. Merola ◽  
T. L. Clanton
Keyword(s):  
Contractile Function ◽  
Force Production ◽  
Creatine Phosphate ◽  
High Energy ◽  
Diaphragm Muscle ◽  
Severe Hypoxia ◽  
High Energy Phosphates ◽  
Rat Diaphragm ◽  
Tetanic Force ◽  
Hypoxia Exposure

Acute exposure to severe hypoxia depresses contractile function and induces adaptations in skeletal muscle that are only partially understood. Previous studies have demonstrated that antioxidants (AOXs) given during hypoxia partially protect contractile function, but this has not been a universal finding. This study confirms that specific AOXs, known to act primarily as superoxide scavengers, protect contractile function in severe hypoxia. Furthermore, the hypothesis is tested that the mechanism of protection involves preservation of high-energy phosphates (ATP, creatine phosphate) and reductions of Pi. Rat diaphragm muscle strips were treated with AOXs and subjected to 30 min of hypoxia. Contractile function was examined by using twitch and tetanic stimulations and the degree of elevation in passive force occurring during hypoxia (contracture). High-energy phosphates were measured at the end of 30-min hypoxia exposure. Treatment with the superoxide scavengers 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron, 10 mM) or Mn(III)tetrakis(1-methyl-4-pyridyl) porphyrin pentachloride (50 μM) suppressed contracture during hypoxia and protected maximum tetanic force. N-acetylcysteine (10 or 18 mM) had no influence on tetanic force production. Contracture during hypoxia without AOXs was also shown to be dependent on the extracellular Ca2+ concentration. Although hypoxia resulted in only small reductions in ATP concentration, creatine phosphate concentration was decreased to ∼10% of control. There were no consistent influences of the AOX treatments on high-energy phosphates during hypoxia. The results demonstrate that superoxide scavengers can protect contractile function and reduce contracture in hypoxia through a mechanism that does not involve preservation of high-energy phosphates.

Exercise hyperthermia as a factor limiting physical performance: temperature effect on muscle metabolism

1985 ◽  
Vol 59 (3) ◽  
pp. 766-773 ◽  
Author(s):  
S. Kozlowski ◽  
Z. Brzezinska ◽  
B. Kruk ◽  
H. Kaciuba-Uscilko ◽  
J. E. Greenleaf ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Muscle Metabolism ◽  
Creatine Phosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Glycogen Depletion ◽  
Heavy Exercise ◽  
High Energy Phosphate ◽  
Glycolytic Intermediates ◽  
Temperature Equilibrium

The muscle contents of high-energy phosphates and their derivatives [ATP, ADP, AMP, creatine phosphate (CrP), and creatine], glycogen, some glycolytic intermediates, pyruvate, and lactate were compared in 11 dogs performing prolonged heavy exercise until exhaustion (at ambient temperature 20.0 +/- 1.0 degrees C) without and with trunk cooling using ice packs. Without cooling, dogs were able to run for 57 +/- 8 min, and their rectal (Tre) and muscle (Tm) temperatures increased to 41.8 +/- 0.2 and 43.0 +/- 0.2 degrees C, respectively. Compared with noncooling, duration of exercise with cooling was longer by approximately 45% while Tre and Tm at the time corresponding to the end of exercise without cooling were lower by 1.1 +/- 0.2 and 1.2 +/- 0.2 degrees C, respectively. The muscle contents of high-energy phosphates (ATP + CrP) decreased less, the rate of glycogen depletion was lower, and the increases in the contents of AMP, pyruvate, and lactate as well as in the muscle-to-blood lactate ratio were smaller. The muscle content of lactate was positively correlated with Tm. The data indicate that with higher body temperature equilibrium between high-energy phosphate breakdown and resynthesis was shifted to the lower values of ATP and CrP and glycolysis was accelerated. The results suggest that hyperthermia developing during prolonged muscular work exerts an adverse effect on muscle metabolism that may be relevant to limitation of endurance.

Abstract 1571: Hibernating Myocardium has Reduced High Energy Phosphate Levels and a Preconditioning-Like Effect with Slower ATP Depletion in Response to Acute Ischemia

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Qingsong Hu ◽  
Gen Suzuk ◽  
John M Canty ◽  
James A Fallavollita
Keyword(s):  
High Energy ◽  
Atp Depletion ◽  
Energy Utilization ◽  
Hibernating Myocardium ◽  
Wall Thickening ◽  
Acute Ischemia ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Chronic Coronary Artery Disease ◽  
Atp Levels

Background. Pigs with a chronic LAD stenosis develop hibernating myocardium with contractile dysfunction and reduced resting flow. We hypothesized that this reduced energy utilization preserves ATP and protects the heart from irreversible injury during acute ischemia. Methods. Pigs with hibernating myocardium were studied 3-months after instrumentation with a 1.5 mm proximal LAD stenosis (n=7). Hibernating myocardium was confirmed by reduced LAD wall thickening (2.4±0.2 vs.6.1±0.6 mm in remote, p<0.05) and reduced resting flow (0.95±0.15 vs. 1.66±0.29 ml/min/g in remote, p<0.05) without infarction. Subendocardial samples were rapidly excised from propofol anesthetized pigs and serial depletion of high energy phosphates quantified by HPLC (in μmol/g dry weight) during simulated total ischemia in vitro (37°C). Results. At Baseline, ATP and ADP were significantly reduced in the hibernating LAD region in comparison to controls (n=8, Table ), with preserved CP/ATP and ATP/ADP ratios. During simulated ischemia, hibernating myocardium displayed a markedly reduced rate of ATP depletion (ΔATP), with ATP levels at 20 min significantly higher than control (Table ). Higher ATP levels were maintained throughout 80 min of ischemia. Interestingly, identical preservation of high energy phosphates occurred in the remote normally perfused region of hearts with hibernating myocardium (Table ). Conclusion. These data indicate that there is a balanced reduction in high energy phosphate levels in hibernating myocardium with chronic protection from ischemia manifested by a slower rate of ATP depletion during acute ischemia. This preconditioning-like effect is global suggesting that it arises from stimuli that are not directly related to ischemia. This raises the possibility that stretch from cyclical elevations in LV filling pressure or a circulating factor released from the heart in response to ischemia can protect the heart in chronic coronary artery disease.

scholarly journals Modulation of Glutamate-Induced Intracellular Energy Failure in Neonatal Cerebral Cortical Slices by Kynurenic Acid, Dizocilpine, and NBQX

1994 ◽  
Vol 14 (2) ◽  
pp. 269-278 ◽  
Author(s):  
Maryceline T. Espanol ◽  
Yan Xu ◽  
Lawrence Litt ◽  
Guo-Yuan Yang ◽  
Lee-Hong Chang ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Kynurenic Acid ◽  
High Energy ◽  
High Energy Phosphates ◽  
Sprague Dawley ◽  
High Energy Phosphate ◽  
Additional Energy ◽  
Atp Levels ◽  
Cortical Slices ◽  
Energy Failure

The severity and rapidity of acute, glutamate-induced energy failure were compared in live cerebral cortical slices. In each experiment 80 live cerebral cortical slices (350 μm thick) were obtained from neonatal Sprague–Dawley rats, suspended and perfused in a nuclear magnetic resonance (NMR) tube, and studied at 4.7 T with interleaved 31P/1H NMR spectroscopy. NMR spectra, obtained continually, were determined as 5-min averages. Slices were perfused for 60 min with artificial cerebrospinal fluid (ACSF) containing either glutamate alone or glutamate mixed with one of three glutamate-receptor antagonists: kynurenate, dizocilpine (MK-801), and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo( F)quinoxaline (NBQX). Dose-dependent decreases in high-energy phosphates were studied during glutamate exposure (0.5 to 10 m M), with and without antagonist protection. Energy recovery after glutamate exposures was measured during a 60-min washout with glutamate-free, antagonist-free ACSF. Reversible and irreversible energy failures were characterized by changes in intracellular pH, and by changes in relative concentrations of ATP, phosphocreatine (PCr), and inorganic phosphate. No changes were observed in intracellular levels of N-acetylaspartate and lactate. Some special studies were also done using R-(–)-2-amino-5-phosphonovaleric acid (100 μ M) and tetrodotoxin (1 m M) to examine glutamate receptor specificity in this tissue model. Dizocilpine (150 μ M) best ameliorated the energy failure caused by 2.0 m M glutamate. With dizocilpine the maximum ATP decrease was only 6 ± 5%, instead of 35 ± 7%. Additionally, the dizocilpine-induced recovery of ATP levels, complete after 30 min of glutamate exposure, lasted througout 30 additional min of glutamate exposure and 60 additional min of washout with glutamate-free ACSF. Although dizocilpine did not alter the maximum decrease that occurred in PCr (to 36 ± 4% of control), dizocilpine did cause PCr levels to return to within 7 ± 5% of the control after 30 min of glutamate exposure. PCr levels stayed at this value throughout 30 additional min of glutamate exposure. During the washout period PCr immediately rose to a value 5 ± 2% above the control and then remained constant during the rest of the 60-min washout. During the first 20 min of glutamate administration, kynurenic acid (1.0 m M) best improved the high-energy phosphate levels. NBQX (6.0 μ M), reported to protect the brain from ischemic injury, decreased PCr depletion during glutamate exposure without affecting the loss of ATP. After 60 min of glutamate washout, PCr levels with kynurenate (84 ± 6% of control) and NBQX (84 ± 2% of control) were significantly higher (p < 0.001) than with glutamate alone (42 ± 6% of control), although ATP levels were not significantly improved by either drug. Acute energy failure in our brain slice model, intended to simulate oxygenated penumbral tissue, probably occurs primarily in neurons. The reason that dizocilpine best preserves high-energy phosphate levels might relate to its mechanism of N-methyl-d-aspartate receptor blockade. Additional energy protection from dizocilpine might also arise from a partial blockade of voltage-dependent Na+ channels, which is possible at the concentration used.

31P-NMR measurements of pHi and high-energy phosphates in isolated turtle hearts during anoxia and acidosis

1990 ◽  
Vol 259 (3) ◽  
pp. R521-R530 ◽  
Author(s):  
J. S. Wasser ◽  
K. C. Inman ◽  
E. A. Arendt ◽  
R. G. Lawler ◽  
D. C. Jackson
Keyword(s):  
Heart Rate ◽  
Lactic Acidosis ◽  
Cardiac Function ◽  
31P Nmr ◽  
Creatine Phosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Atp Levels ◽  
Pressure Development ◽  
Developed Pressure

We used 31P-nuclear magnetic resonance (NMR) spectroscopy to measure intracellular pH (pHi) and high-energy phosphate levels in hearts of turtles (Chrysemys picta bellii) during either 4 h of anoxia [extracellular pH (pHo) 7.8, 97% N2-3% CO2], 4 h of lactic acidosis (pHo 7.0, 97% O2-3% CO2), or 1.5 h of combined anoxia + lactic acidosis (pHo 7.0, 97% N2-3% CO2) followed by 2 h of oxygenated recovery (pHo 7.8) at 20 degrees C. We also measured heart rate, maximum ventricular-developed pressure, and rate of pressure development (dP/dtmax). 31P-NMR spectra were characterized by the seven peaks typical of mammalian hearts, although turtle spectra were dominated by a large phosphodiester peak. Anoxia caused an increase in Pi to 165% and a decrease in creatine phosphate (CP) to 42% of control, whereas ATP levels remained unchanged. pHi declined from 7.37 +/- 0.01 to 7.22 +/- 0.03 at 1 h of anoxia and remained unchanged through hour 4. Lactic acidosis caused a 59% decrease in Pi, whereas CP and ATP levels remained unchanged. pHi fell to 6.88 +/- 0.04 by hour 1 and then climbed steadily to 7.14 +/- 0.05 at hour 4. During recovery from acidosis, pHi exceeded control values and returned to control by 2 h. Combined anoxia + acidosis caused profound decreases in CP to 14% and pHi to 6.56 +/- 0.03. In anoxic hearts, cardiodynamic variables remained at control levels through hour 3, after which cardiac output, heart rate, and dP/dtmax declined. Cardiodynamic variables were essentially unchanged from control throughout 4 h of acidosis except for dP/dtmax, which declined rapidly. In the combined protocol, all measures of cardiac function decreased. Recovery in all three cases was complete by approximately 2 h. We conclude that turtle hearts were relatively resistant to the stresses imposed in all three protocols compared with mammalian hearts, although anoxia + acidosis depressed the measured cardiac variables more profoundly than predicted from responses to the conditions imposed separately. Our results from the anoxia protocol suggest no direct causal relationship between myocardial CP (or ATP) levels and cardiac function.

Ischemic cardioprotection by ATP-sensitive K+ channels involves high-energy phosphate preservation

1993 ◽  
Vol 265 (5) ◽  
pp. H1809-H1818 ◽  
Author(s):  
C. D. McPherson ◽  
G. N. Pierce ◽  
W. C. Cole
Keyword(s):  
Guinea Pig ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Creatine Phosphate ◽  
High Energy ◽  
Mechanical Activity ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
K Channels ◽  
Ischemic Contracture

We previously demonstrated that ATP-sensitive K+ channels (KATP) protect the guinea pig myocardium against ischemia-reperfusion injury (Cole et al., Circ. Res. 69: 571-581, 1991), but the cellular alterations leading to ischemic injury affected by KATP remain to be defined. This study investigates the relationship between activation of KATP and preservation of high-energy phosphates during global no-flow ischemia in arterially perfused guinea pig right ventricular walls. Electrical and mechanical activity were recorded via intracellular microelectrodes and a force transducer. Glibenclamide (10 and 50 microM) and pinacidil (10 microM) were used to modulate KATP. ATP and creatine phosphate (CP) levels were determined at the end of no-flow ischemia by enzymatic analysis. Preparations were subjected to 1) 20 min no-flow +/- glibenclamide (10 or 50 microM), 2) 30 min no-flow +/- pinacidil (10 microM) or pinacidil (10 microM) and glibenclamide (50 microM), or 3) 40 or 50 min of control perfusion before rapid freezing in liquid nitrogen. Pinacidil (10 microM) enhanced ischemic shortening of action potential duration (APD) and early contractile failure, prevented ischemic contracture, and inhibited high-energy phosphate depletion during ischemia. Glibenclamide (50 microM) inhibited the effects of pinacidil (10 microM) on electromechanical function and preservation of ATP and CP. Glibenclamide (10 microM) alone inhibited the early decline in APD and produced earlier ischemic contracture but did not enhance ATP or CP depletion compared with untreated tissues during 20 min of no-flow. Glibenclamide (50 microM) produced a greater inhibition of APD shortening in early ischemia, further decreased the latency to ischemic contracture, and caused enhanced ischemic depletion of ATP. The data indicate the changes in electrical activity induced by KATP indirectly preserve high-energy phosphates and reduce injury associated with ischemia. However, the data also suggest the possible presence of additional mechanisms for cardioprotection by KATP.

Responses of beta-adrenoceptor in rat soleus to phosphorus compound levels and/or unloading

1994 ◽  
Vol 266 (5) ◽  
pp. C1257-C1262 ◽  
Author(s):  
Y. Ohira ◽  
K. Saito ◽  
T. Wakatsuki ◽  
W. Yasui ◽  
T. Suetsugu ◽  
...  
Keyword(s):  
Contractile Activity ◽  
Creatine Supplementation ◽  
High Energy ◽  
Hindlimb Suspension ◽  
Phosphorus Compounds ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Gravitational Unloading ◽  
Beta Adrenoceptor ◽  
Muscle Contractile

Responses of beta-adrenoceptor (beta-AR) in rat soleus to gravitational unloading and/or changes in the levels of phosphorus compounds by feeding either creatine or its analogue beta-guanidinopropionic acid (beta-GPA) were studied. A decrease in the density of beta-AR (about -35%) was induced by 10 days of hindlimb suspension, but the affinity of the receptor was unaffected. Suspension unloading tended to increase the levels of adenosine triphosphate and phosphocreatine and decrease inorganic phosphate. Even without unloading, the beta-AR density decreased after an oral creatine supplementation (about -20%), which also tended to elevate the high-energy phosphate levels in muscle. However, an elevation of beta-AR density was induced (about +36%) after chronic depletion of high-energy phosphates by feeding beta-GPA (about +125%). Data suggest that the density of beta-AR in muscle is elevated if the high-energy phosphate contents are chronically decreased and vice versa. However, it may not be directly related to the degree of muscle contractile activity.

Cellular K+ loss and anion efflux during myocardial ischemia and metabolic inhibition

1989 ◽  
Vol 256 (4) ◽  
pp. H1165-H1175 ◽  
Author(s):  
J. N. Weiss ◽  
S. T. Lamp ◽  
K. I. Shine
Keyword(s):  
Inorganic Phosphate ◽  
Lactate Production ◽  
Selective Inhibition ◽  
High Energy ◽  
Metabolic Inhibitors ◽  
Charge Movement ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Myocardial Hypoxia ◽  
Inhibition Of Glycolysis

It has been suggested that increased K+ efflux during myocardial hypoxia and ischemia may result from efflux of intracellularly generated anions such as lactate and inorganic phosphate (Pi) as a mechanism of balancing transsarcolemmal charge movement. To investigate this hypothesis cellular K+ loss using 42K+ and K+-sensitive electrodes, intracellular potential, venous lactate and Pi, and tissue lactate and high-energy phosphates were measured in isolated arterially perfused rabbit interventricular septa during exposure to metabolic inhibitors, hypoxia, and ischemia. Selective inhibition of glycolysis caused a marked increase in K+ efflux despite a fall in lactate production and maintenance of normal cellular high-energy phosphate content. During ischemia and hypoxia net loss of lactate and Pi exceeded K+ loss by a factor of 2-6. However, removal of glucose prior to ischemia or during hypoxia increased K+ loss but reduced lactate loss without affecting Pi loss. During hypoxia, 30 mM exogenous lactate did not alter K+ loss in a manner consistent with changes in passive electrodiffusion of lactate ion. These findings inhibition which is not related to anion efflux assumes greater importance under conditions in which glycolysis is inhibited, e.g., ischemia. Under conditions in which glycolysis is not inhibited, e.g., hypoxia, K+ efflux does not parallel passive electrodiffusion of lactate ions. However, this finding does not exclude the possibility that K+ loss could be coupled to carrier-mediated lactate ion efflux.

Anaerobic energy provision in aged skeletal muscle during tetanic stimulation

1991 ◽  
Vol 70 (4) ◽  
pp. 1787-1795 ◽  
Author(s):  
C. B. Campbell ◽  
D. R. Marsh ◽  
L. L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Energy Demand ◽  
Energy Charge ◽  
High Energy ◽  
High Energy Phosphates ◽  
Fischer 344 ◽  
Charge Potential ◽  
Anaerobic Energy ◽  
Gastrocnemius Muscles

The effect of age on skeletal muscle anaerobic energy metabolism was investigated in adult (11 mo) and aged (25 mo) Fischer 344 rats. Hindlimb skeletal muscles innervated by the sciatic nerve were stimulated to contract with trains of supramaximal impulses (100 ms, 80 Hz) at a train rate of 1 Hz for 60 s, with an occluded circulation. Soleus, plantaris, and red and white gastrocnemius (WG) were sampled from control and stimulated limbs. All muscle masses were reduced with age (9-13%). Peak isometric tensions, normalized per gram of wet muscle, were lower throughout the stimulation in the aged animals (28%). The potential for anaerobic ATP provision was unaltered with age in all muscles, because resting high-energy phosphates and glycogen contents were similar to adult values. Anaerobic ATP provision during stimulation was unaltered by aging in soleus, plantaris, and red gastrocnemius muscles. In the WG, containing mainly fast glycolytic (FG) fibers, ATP and phosphocreatine contents were depleted less in aged muscle. In situ glycogenolysis and glycolysis were 90.0 +/- 4.8 and 69.3 +/- 2.6 mumol/g dry muscle (dm) in adult WG and reduced to 62.3 +/- 6.9 and 51.5 +/- 5.5 mumol/g dm, respectively, in aged WG. Consequently, total anaerobic ATP provision was lower in aged WG (224.5 +/- 20.9 mumol/g dm) vs. adult (292.6 +/- 7.6 mumol/g dm) WG muscle. In summary, the decreased tetanic tension production in aged animals was associated with a decreased anaerobic energy production in FG fibers. Reduced high-energy phosphate use and a greater energy charge potential after stimulation suggested that the energy demand was reduced in aged FG fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

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