THE INFLUENCE OF SYMPATHOMIMETIC AMINES, MONOAMINE OXIDASE INHIBITORS, AND ANTIHYPERTENSIVES UPON THE ENERGY METABOLISM IN THE RAT HEART

1966 ◽  
Vol 44 (4) ◽  
pp. 605-613 ◽  
Author(s):  
W. G. Hilliard ◽  
W. T. Oliver ◽  
G. R. Van Petten
Keyword(s):  
Energy Metabolism ◽  
Monoamine Oxidase ◽  
Rat Heart ◽  
Antihypertensive Drugs ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Monoamine Oxidase Inhibitors ◽  
Sympathomimetic Amines ◽  
Cardiac Energy Metabolism

This investigation was undertaken to determine the effects of three classes of catecholamine-releasing drugs on cardiac energy metabolism. The levels of adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), inorganic phosphate (IP), and phosphocreatine (CP) of the rat heart were measured. The sympathomimetic amines tyramine, ephedrine, methylamphetamine, and (+)- and (−)-amphetamine caused significant decreases in CP. Tyramine and (+)- and (−)-amphetamine also significantly depressed ATP. Of the antihypertensive drugs investigated, bretylium and guanethidine decreased the amount of CP present, and the latter compound also significantly decreased ATP. The administration of reserpine was without significant effect on cardiac high-energy phosphate levels. Among the monoamine oxidase inhibitors, tranylcypromine significantly lowered ATP and CP, whereas pheniprazine produced no significant changes. This study showed that those drugs which have been reported to release cardiac catecholamines also reduced cardiac levels of CP and ATP. The hypothesis is advanced that this effect is due to increased utilization of energy by two mechanisms: (a) stimulation of the active recapture mechanism for adrenergic neurotransmitters, and (b) the positive inotropic and chronotropic responses of the heart to the drug-released catecholamines. In either case, the observed decreases in the levels of ATP and CP in the heart are effects of sympathomimetic amines which have been heretofore unreported.

PHOSPHORYLATION COUPLED TO THE OXIDATION OF SULFITE AND 2-MERCAPTOETHANOL IN EXTRACTS OF THIOBACILLUS THIOPARUS

1967 ◽  
Vol 13 (7) ◽  
pp. 873-884 ◽  
Author(s):  
E. A. Davis ◽  
E. J. Johnson
Keyword(s):  
Electron Donor ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Thiobacillus Thioparus ◽  
Ph Values ◽  
Cell Extracts ◽  
Endogenous Level ◽  
Sulfite Oxidation

The effect of 10−4 M 2, 4-dinitrophenol (DNP) on the production of high energy phosphate bonds during sulfite and 2-mercaptoethanol (2-ME) oxidation by cell extracts of Thiobacillus thioparus was determined. Phosphorylation was measured indirectly by14CO2fixation and directly by32PO4esterification. DNP-sensitive phosphorylation was demonstrated by coupling sulfite oxidation with the concomitant phosphorylation of adenosine monophosphate (AMP) to14CO2fixation beginning with ribose-5-phosphate. Esterification of32PO4was measured at pH values of 6.4, 7.2, and 8.0 with AMP and adenosine diphosphate (ADP) as the phosphate acceptor and sulfite as the electron donor. The optimal pH for the greatest DNP-sensitive phosphorylation was 7.2 with AMP. DNP at 10−4 M significantly reduced32PO4esterification at all pH values tested and with the three ADP concentrations employed. Maximum DNP-sensitive phosphorylation of ADP was demonstrated with 5 μmoles of ADP at pH 7.2. The maximum P:O ratio was 0.13. With 2-ME as the nonphysiological electron donor and AMP as the phosphate acceptor, no phosphorylation above the endogenous level was measured at the three pH values tested. With ADP as the phosphate acceptor and 2-ME as the electron donor,32PO4esterification significantly above the endogenous level was demonstrated at pH 6.4 with 5 μmoles of ADP; this phosphorylation was sensitive to 10−4 M DNP.

scholarly journals Amelioration of Energy Metabolism by Melatonin in Skeletal Muscle of Rats With LPS Induced Endotoxemia

2016 ◽  
pp. 833-842 ◽  
Author(s):  
E. OZKOK ◽  
H. YORULMAZ ◽  
G. ATES ◽  
A. AKSU ◽  
N. BALKIS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Muscle Tissue ◽  
High Performance ◽  
Succinic Dehydrogenase ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Creatine Phosphate ◽  
Before And After ◽  
Hematoxylin And Eosin

In the literature, few studies have investigated the effects of melatonin on energy metabolism in skeletal muscle in endotoxemia. We investigated the effects of melatonin on tissue structure, energy metabolism in skeletal muscle, and antioxidant level of rats with endotoxemia. We divided rats into 4 groups, control, lipopolysaccharide (LPS) (20 mg/kg, i.p., single dose), melatonin (10 mg/kg, i.p., three times), and melatonin + LPS. Melatonin was injected i.p. 30 min before and after the 2nd and 4th hours of LPS injection. Antioxidant status was determined by glutathione (GSH) measurement in the blood. Muscle tissue was stained using modified Gomori trichrome (MGT), succinic dehydrogenase (SDH), and cytochrome oxidase (COX) and histological scored. Also the sections were then stained with hematoxylin and eosin. The stained sections were visualized and photographed. Creatine, creatine phosphate, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels were investigated using high performance liquid chromatography (HPLC) in muscle tissue. In the Melatonin + LPS group, blood GSH levels were increased compared with the LPS group (P<0.01). Melatonin reduced myopathic changes in the LPS group according to the histopathologic findings. In addition, ATP values were increased compared with the LPS group (P<0.05). Our findings showed melatonin treatment prevented muscle damage by increasing ATP and GSH levels in rats with LPS induced endotoxemia.

Temporal profile and significance of metabolic failure and trophic changes in the canine cerebral arteries during chronic vasospasm after subarachnoid hemorrhage

1993 ◽  
Vol 78 (5) ◽  
pp. 807-812 ◽  
Author(s):  
Yuhei Yoshimoto ◽  
Phyo Kim ◽  
Tomio Sasaki ◽  
Kintomo Takakura
Keyword(s):  
Subarachnoid Hemorrhage ◽  
High Performance ◽  
Close Association ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphates ◽  
Content Type ◽  
Temporal Profile

✓ To investigate the pathogenetic significance of metabolic failure observed in spastic cerebral arteries after subarachnoid hemorrhage (SAH), the temporal profile of alterations in the arterial content of high-energy phosphates was studied. A canine model of double hemorrhage was used. Constriction of the basilar artery was measured angiographically on Days 3, 5, 7, and 14 after SAH in separate groups of animals. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), guanosine triphosphate (GTP), guanosine diphosphate, creatine phosphate (CrP), and creatine (Cr) levels in the arteries were assayed using high-performance liquid chromatography. A time-dependent development of angiographic spasm was confirmed. A mild vasospasm was seen in the group studied 3 days after SAH, progressed in the Day 5 group, remained comparably severe in the Day 7 group, and resolved partially in the Day 14 group. The content of high-energy phosphates (ATP, GTP, and CrP) declined rapidly over the course of the study, and a significant reduction in ATP, GTP, and CrP was observed in the Day 3 group. Levels of ATP and CrP decreased further in the Day 5 and 7 groups. The decrement in GTP was completed in the early phase; a significant reduction took place in the Day 3 group, with no progression thereafter and no recovery though Day 14. Total adenylate (ATP + ADP + AMP) and total creatine (Cr + CrP) content diminished markedly over the course of the study. These results indicate that metabolic failure and trophic disturbance in the cerebral artery occurs with a rapid onset following SAH and progresses in close association with the development of vasospasm, suggesting a significant causal relationship with the pathogenesis.

Effects of ACE inhibition and β-receptor blockade on energy metabolism in rats postmyocardial infarction

1999 ◽  
Vol 277 (6) ◽  
pp. H2167-H2175 ◽  
Author(s):  
Stephanie Hügel ◽  
Michael Horn ◽  
Mark de Groot ◽  
Helga Remkes ◽  
Charlotte Dienesch ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ace Inhibitors ◽  
High Energy ◽  
Left Ventricular ◽  
Reaction Velocity ◽  
Cardiac Energy Metabolism ◽  
Receptor Blockers ◽  
Cardiac Energy ◽  
Total Creatine ◽  
Β Receptor

Chronic treatment with β-receptor blockers or angiotensin-converting enzyme (ACE) inhibitors in heart failure can reduce mortality and improve left ventricular function, but the mechanisms involved in their beneficial action remain to be fully defined. Our hypothesis was that these agents prevent the derangement of cardiac energy metabolism. Rats were subjected to myocardial infarction (MI) or sham operation. Thereafter, animals were treated with bisoprolol, captopril, or remained untreated. Two months later, cardiac function was measured in the isolated heart by a left ventricular balloon (pressure-volume curves), and energy metabolism of residual intact myocardium was analyzed in terms of total and isoenzyme creatine kinase (CK) activity, steady-state levels (ATP, phosphocreatine), and turnover rates (CK reaction velocity) of high-energy phosphates (31P nuclear magnetic resonance) and total creatine content (HPLC). Bisoprolol and partially captopril prevented post-MI hypertrophy and partially prevented left ventricular contractile dysfunction. Residual intact failing myocardium in untreated, infarcted hearts showed a 25% decrease of the total, a 26% decrease of MM-, and a 37% decrease of the mitochondrial CK activity. Total creatine was reduced by 15%, phosphocreatine by 21%, and CK reaction velocity by 41%. Treatment with bisoprolol or captopril largely prevented all of these changes in infarcted hearts. Thus the favorable functional effects of β-receptor blockers and ACE inhibitors post-MI are accompanied by substantial beneficial effects on cardiac energy metabolism.

INFLUENCE OF INGESTED CASEIN HYDROLYZATE ON THE HIGH ENERGY NUCLEOTIDE CONTENT OF WORKING MUSCLE

1963 ◽  
Vol 41 (1) ◽  
pp. 1531-1536
Author(s):  
J. M. Afar ◽  
V. A. Rogozkin
Keyword(s):  
Amino Acids ◽  
Phosphoric Acid ◽  
Low Temperatures ◽  
Muscular Activity ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
Albino Rats ◽  
Phosphate Ester ◽  
Casein Hydrolyzate

The results of experiments carried out on albino rats show that administration, during periods of continued muscular activity, of casein hydrolyzate, a mixture of amino acids, or phosphoric acid salts, favors the maintenance of a higher than normal level of adenosine triphosphate (ATP) and phosphocreatine (CP) and a corresponding decrease in the level of adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in the muscles.It appears from this study that just as carbohydrate is known to have a protein-sparing action, so amino acids have been found to have a sparing action in the metabolism of carbohydrate and phosphate ester in the animal even under conditions of intense physical exercise at low temperatures.

High-energy phosphate levels in the cerebral artery during chronic vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (6) ◽  
pp. 991-996 ◽  
Author(s):  
Phyo Kim ◽  
James D. Jones ◽  
Thoralf M. Sundt
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
High Performance ◽  
Venous Blood ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Content Type ◽  
Chronic Vasospasm

✓ High-energy phosphate levels were measured in the canine cerebral artery during chronic vasospasm. Subarachnoid hemorrhage and vasospasm were induced by percutaneous injections of autologous venous blood into the cisterna magna. Narrowing of the artery was confirmed by angiography 7 days later. Levels of adenosine phosphates (adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP)), guanosine phosphates (guanosine triphosphate (GTP) and guanosine diphosphate (GDP)), and creatine phosphate (CrP) in the basilar artery were quantified using high-performance liquid chromatography. The total creatine (Crtotal) content was measured by a spectrophotometric method after acid hydrolysis of CrP. Levels of ATP, GTP, and CrP were markedly reduced in the spastic arteries, and ratios of ATP:ADP, GTP:GDP, and CrP:Crtotal were significantly decreased. The results indicate a serious disturbance in the energy metabolism that takes place in the cerebral artery during chronic vasospasm.

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