Ketone bodies maintain normal cardiac function and myocardial high energy phosphates during insulin-induced hypoglycemia in vivo

1989 ◽  
Vol 84 (5) ◽  
pp. 510-523 ◽  
Author(s):  
J. Breuer ◽  
K. J. Chung ◽  
E. Pesonen ◽  
R. H. Haas ◽  
B. D. Guth ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ketone Bodies ◽  
High Energy ◽  
High Energy Phosphates ◽  
Normal Cardiac Function

Metabolic and energy correlates of intracellular pH in progressive fatigue of squid (L. brevis) mantle muscle

1996 ◽  
Vol 271 (5) ◽  
pp. R1403-R1414 ◽  
Author(s):  
H. O. Portner ◽  
E. Finke ◽  
P. G. Lee
Keyword(s):  
Free Energy ◽  
Critical Velocity ◽  
Energy Levels ◽  
High Energy ◽  
Swimming Velocity ◽  
High Energy Phosphates ◽  
Energy Status ◽  
Intracellular Acidosis ◽  
Model Calculations

Squid (Lolliguncula brevis) were exercised at increasing swimming speeds to allow us to analyze the correlated changes in intracellular metabolic, acid-base, and energy status of the mantle musculature. Beyond a critical swimming velocity of 1.5 mantle lengths/s, an intracellular acidosis developed that was caused by an initial base loss from the cells, the onset of respiratory acidification, and, predominantly, octopine formation. The acidosis was correlated with decreasing levels of phospho-L-arginine and, thus, supported ATP buffering at the expense of the phosphagen. Monohydrogenphosphate, the actual substrate of glycogen phosphorylase accumulated, enabling glycogen degradation, despite progressive acidosis. In addition to octopine, succinate, and glycerophosphate accumulation, the onset of acidosis characterizes the critical velocity and indicates the transition to a non-steady-state time-limited situation. Accordingly, swimming above the critical velocity caused cellular energy levels (in vivo Gibbs free energy change of ATP hydrolysis) to fall. A minimal value was reached at about -45 kJ/mol. Model calculations demonstrate that changes in free Mg2+ levels only minimally affect ATP free energy, but minimum levels are relevant in maintaining functional concentrations of Mg(2+)-complexed adenylates. Model calculations also reveal that phosphagen breakdown enabled L. brevis to reach swimming speeds about three times higher than the critical velocity. Comparison of two offshore squid species (Loligo pealei and Illex illecebrosus) with the estuarine squid L.brevis indicates that the latter uses a strategy to delay the exploitation of high-energy phosphates and protect energy levels at higher than the minimum levels (-42 kJ/mol) characterizing fatigue in the other species. A more economical use of anaerobic resources and an early reduction in performance may enable L. brevis to tolerate more extreme environmental conditions in shallow estuarine waters and even hypoxic environments and to prevent a fatal depletion of energy stores.

Carbofuran-induced alterations (in vivo) in high-energy phosphates, creatine kinase (CK) and CK isoenzymes

1991 ◽  
Vol 65 (4) ◽  
pp. 304-310 ◽  
Author(s):  
Ramesh C. Gupta ◽  
John T. Goad ◽  
Wade L. Kadel
Keyword(s):  
Creatine Kinase ◽  
High Energy ◽  
High Energy Phosphates

scholarly journals Transplantation of autologously derived mitochondria protects the heart from ischemia-reperfusion injury

2013 ◽  
Vol 304 (7) ◽  
pp. H966-H982 ◽  
Author(s):  
Akihiro Masuzawa ◽  
Kendra M. Black ◽  
Christina A. Pacak ◽  
Maria Ericsson ◽  
Reanne J. Barnett ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Reperfusion Injury ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Energy ◽  
Creatine Kinase Mb ◽  
Myocardial Energetics

Mitochondrial damage and dysfunction occur during ischemia and modulate cardiac function and cell survival significantly during reperfusion. We hypothesized that transplantation of autologously derived mitochondria immediately prior to reperfusion would ameliorate these effects. New Zealand White rabbits were used for regional ischemia (RI), which was achieved by temporarily snaring the left anterior descending artery for 30 min. Following 29 min of RI, autologously derived mitochondria (RI-mitochondria; 9.7 ± 1.7 × 106/ml) or vehicle alone (RI-vehicle) were injected directly into the RI zone, and the hearts were allowed to recover for 4 wk. Mitochondrial transplantation decreased ( P < 0.05) creatine kinase MB, cardiac troponin-I, and apoptosis significantly in the RI zone. Infarct size following 4 wk of recovery was decreased significantly in RI-mitochondria (7.9 ± 2.9%) compared with RI-vehicle (34.2 ± 3.3%, P < 0.05). Serial echocardiograms showed that RI-mitochondria hearts returned to normal contraction within 10 min after reperfusion was started; however, RI-vehicle hearts showed persistent hypokinesia in the RI zone at 4 wk of recovery. Electrocardiogram and optical mapping studies showed that no arrhythmia was associated with autologously derived mitochondrial transplantation. In vivo and in vitro studies show that the transplanted mitochondria are evident in the interstitial spaces and are internalized by cardiomyocytes 2–8 h after transplantation. The transplanted mitochondria enhanced oxygen consumption, high-energy phosphate synthesis, and the induction of cytokine mediators and proteomic pathways that are important in preserving myocardial energetics, cell viability, and enhanced post-infarct cardiac function. Transplantation of autologously derived mitochondria provides a novel technique to protect the heart from ischemia-reperfusion injury.

The effect of an adenosine and lidocaine intravenous infusion on myocardial high-energy phosphates and pH during regional ischemia in the rat model in vivo

2006 ◽  
Vol 84 (8-9) ◽  
pp. 903-912 ◽  
Author(s):  
Sarah J. Canyon ◽  
Geoffrey P. Dobson
Keyword(s):  
Body Mass ◽  
Rat Model ◽  
Intravenous Infusion ◽  
High Energy ◽  
Coronary Artery Ligation ◽  
Ischemia And Reperfusion ◽  
High Energy Phosphates ◽  
Regional Ischemia ◽  
Significant Difference

We have previously shown that an intravenous infusion of adenosine and lidocaine (AL) solution protects against death and severe arrhythmias and reduces infarct size in the in vivo rat model of regional ischemia. The aim of this study was to examine the relative changes of myocardial high-energy phosphates (ATP and PCr) and pH in the left ventricle during ischemia–reperfusion using 31P NMR in AL-treated rats (n = 7) and controls (n = 6). The AL solution (A: 305 μg·(kg body mass)–1·min–1; L: 608 μg·(kg body mass)–1·min–1) was administered intravenously 5 min before and during 30 min coronary artery ligation. Two controls died from ventricular fibrillation; no deaths were recorded in AL-treated rats. In controls that survived, ATP fell to 73% ± 29% of baseline by 30 min ischemia and decreased further to 68% ± 28% during reperfusion followed by a sharp recovery at the end of the reperfusion period. AL-treated rats maintained relatively constant ATP throughout ischemia and reperfusion ranging from 95% ± 6% to 121% ± 10% of baseline. Owing to increased variability in controls, these results were not found to be significant. In contrast, control [PCr] was significantly reduced in controls compared with AL-treated rats during ischemia at 10 min (68% ± 7% vs. 99% ± 6%), at 15 min (68% ± 10% vs. 93% ± 2%), and at 20 min (67% ± 15% vs. 103% ± 5%) and during reperfusion at 10 min (56% ± 22% vs. 99% ± 7%), at 15 min (60% ± 10% vs. 98% ± 7%), and at 35 min (63% ± 14% vs. 120% ± 11%) (p < 0.05). Interestingly, changes in intramyocardial pH between each group were not significantly different during ischemia and fell by about 1 pH unit to 6.6. During reperfusion, pH in AL-treated rats recovered to baseline in 5 min but not in controls, which recovered to only around pH 7.1. There was no significant difference in the heart rate, mean arterial pressure, and rate-pressure product between the controls and AL treatment during ischemia and reperfusion. We conclude that AL cardioprotection appears to be associated with the preservation of myocardial high-energy phosphates, downregulation of the heart at the expense of a high acid-load during ischemia, and with a rapid recovery of myocardial pH during reperfusion.

Efficacy of recombinant human Hb by31P-NMR during isovolemic total exchange transfusion

1999 ◽  
Vol 86 (3) ◽  
pp. 887-894 ◽  
Author(s):  
Laurel O. Sillerud ◽  
Arvind Caprihan ◽  
Nancy Berton ◽  
Gary J. Rosenthal
Keyword(s):  
Exchange Transfusion ◽  
High Energy ◽  
Surface Coil ◽  
High Energy Phosphates ◽  
Significant Drop ◽  
Tissue Ph ◽  
Hb Concentration ◽  
Menten Constant ◽  
Total Exchange

The ability of recombinant human Hb (rHb1.1), which is being developed as an oxygen therapeutic, to support metabolism was measured by in vivo31P-NMR surface coil spectroscopy of the rat abdomen in control animals and in animals subjected to isovolemic exchange transfusion to hematocrit of <3% with human serum albumin or 5 g/dl rHb1.1. No significant changes in metabolite levels were observed in control animals for up to 6 h. The albumin-exchange experiments, however, resulted in a more than eightfold increase in Pi and a 50% drop in phosphocreatine and ATP within 40 min. The tissue pH dropped from 7.4 to 6.8. The decrease in high-energy phosphates obeyed Michaelis-Menten kinetics, with a Michaelis-Menten constant of 3% as the hematocrit at which a 50% drop in high-energy phosphates was observed. Exchange transfusion with rHb1.1 resulted in no significant drop in high-energy phosphates, no rise in Pi, and no change in tissue pH from 7.35 ± 0.15 for up to 5 h after exchange. By these criteria, rHb1.1 at a plasma Hb concentration of ∼5 g/dl after total exchange transfusion was able to sustain energy metabolism of gut tissue at levels indistinguishable from control rats with a threefold higher total Hb level in erythrocytes.

Hypoxic pHi and function modulation by Na+/H+ exchange and alpha-adrenoreceptor inhibition in heart in vivo

1997 ◽  
Vol 272 (6) ◽  
pp. H2664-H2670 ◽  
Author(s):  
M. A. Portman ◽  
Y. Xiao ◽  
B. G. Broers ◽  
X. H. Ning
Keyword(s):  
Cardiac Function ◽  
Contractile Function ◽  
High Energy ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Cardiac Contractile Function ◽  
Significant Drop ◽  
And Function ◽  
Phi Regulation

Regulation of intracellular pH (pHi) may contribute to maintenance of cardiac contractile function during graded hypoxia in vivo. To test this hypothesis, we disturbed pHi regulation in vivo using two approaches: alpha-adrenoreceptor antagonism with phentolamine (1 mg/kg) (Phen; n = 9); and Na+/H+ exchange inhibition with HOE-642 (2 mg/kg; n = 6) before graded hypoxia in open-chest sheep. Hemodynamic parameters including left ventricular maximal pressure development (dP/dtmax) cardiac index (CI), and left ventricular power were monitored continuously and simultaneously with high-energy phosphate levels and pHi, measured with 31P nuclear magnetic resonance spectroscopy in Phen, HOE-642, and control (Con; n = 9). In subgroups (n = 6) in Con and Phen, coronary flow, myocardial oxygen consumption (MVO2), and lactate uptake were also measured. During hypoxia, the functional parameters left ventricular dP/dtmax, CI, and left ventricular power decreased significantly compared with baseline and Con values. These decreases were preceded by a significant drop (P < 0.05) in pHi from 7.10 +/- 0.04 to 6.69 +/- 0.05 in Phen and corresponded temporally to a pHi drop from 7.10 +/- 0.02 to 6.77 +/- 0.03 in HOE-642. Decreases in pHi in Phen were not preceded by decreases in cardiac function or MVO2. In contrast, cardiac function parameters increased significantly in Con, whereas no significant pHi decrease occurred (7.07 +/- 0.03 to 6.98 +/- 0.04). We conclude that these data indicate that pHi regulation can be disrupted through alpha-adrenergic antagonism or Na+/H(+)-exchange inhibition in vivo. These studies demonstrate that pHi regulation performs a role in the modulation of cardiac function during hypoxia in vivo.

Adrenergic influences on cardiac function during ventricular fibrillation in isolated rat hearts

1991 ◽  
Vol 261 (5) ◽  
pp. H1452-H1456
Author(s):  
I. Derad ◽  
I. Funk ◽  
P. Pauschinger ◽  
J. Born
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Ventricular Fibrillation ◽  
Cardiac Function ◽  
Coronary Blood Flow ◽  
High Energy ◽  
High Energy Phosphates ◽  
Tissue Concentrations ◽  
Rat Hearts ◽  
Isolated Rat

Effects of norepinephrine (NE, 10(-6) M), epinephrine (E, 10(-6) M), and vehicle on coronary blood flow (CF), oxygen consumption, and lactate release were compared in 32 isolated rat hearts during 5 min of ventricular fibrillation (VF). After VF, tissue concentrations of ATP, AMP, creatinine phosphate (CP), and lactate were measured. Perfusion of treatments started 30 s after onset of VF and was maintained throughout VF. CF during VF was greater (P less than 0.005) during perfusion of E (mean +/- SE, 5.73 +/- 0.15 ml/min) than NE (5.06 +/- 0.32 ml/min) or vehicle (5.11 +/- 0.18 ml/min). Oxygen consumption during VF was higher during perfusion of E (29.5 +/- 0.9 microliters.min(-1).g wet heart wt(-1)) than vehicle (27.3 +/- 0.7 microliters.min(-1).g(-1); P less than 0.05); average oxygen consumption during NE (27.6 +/- 1.4 microliters.min(-1).g(-1)) and vehicle were comparable. After NE, but not E, tissue AMP concentrations were significantly increased, and CP concentrations were reduced compared with vehicle (P less than 0.05). Enhanced consumption of high-energy phosphates during NE suggests that there is also an enhanced demand for oxygen. However, unlike during E, during NE this demand is not met by an augmented CF. Thus, compared with E, NE treatment during VF may increase the risk of hypoxic damage.

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