scholarly journals Clinical motivation for31P MRS studies on the myocardial energy metabolism of brain dead cats

2003 ◽  
Vol 17 (2-3) ◽  
pp. 503-510
Author(s):  
G. J. Brandon Bravo Bruinsma ◽  
C. J. A. Van Echteld
Keyword(s):  
Energy Metabolism ◽  
Brain Death ◽  
Hemodynamic Instability ◽  
High Energy ◽  
Exclusion Criterion ◽  
High Energy Phosphates ◽  
Myocardial Energy Metabolism ◽  
Brain Dead ◽  
The Brain ◽  
Death Group

Hemodynamic instability of the brain dead potential heart donor is an exclusion criterion for heart donation for transplantation. Based on the results of myocardial biopsies it has been reported that brain death-related catecholamine induced damage of the heart causes depletion of high-energy phosphates which could explain contractile dysfunction. Our group has shown in a series of31P MRS experiments in cats that neither the onset of brain death, nor the hemodynamic deterioration which follows, nor its treatment with high dosages of dopamine affect the heart energetically as expressed by PCr/ATP ratios. However, after cardioplegic arrest and explantation, an initial and prolonged lower ATP content and an anomalous higher PCr/ATP ratio in the brain death group was found when compared with controls during long-term unperfused cold storage of the hearts. During subsequent reperfusion of the hearts, ATP and PCr levels in the brain death group were lower than in controls but equal partial recovery of PCr/ATP ratios was observed in both groups. It was concluded that PCr/ATP ratios need to be interpreted with great caution. Secondly, brain death-related hemodynamic instability is not related to significant changes of myocardial energy metabolism. Thirdly, brain death does affect the myocardial energy metabolism but the impact became apparent only during hypothermic storage and subsequent reperfusion of the donor heart.

In vivo and in vitro31P MRS studies on myocardial energy metabolism of brain dead cats

2000 ◽  
Vol 11 (1) ◽  
pp. 23-26
Author(s):  
G. J. Brandon Bravo Bruinsma ◽  
J. J. Bredée ◽  
T. J. C. Ruigrok ◽  
C. J. A. Echteld
Keyword(s):  
Energy Metabolism ◽  
Myocardial Energy Metabolism ◽  
Brain Dead

Hyperoxia of internal jugular venous blood in brain death

1973 ◽  
Vol 39 (4) ◽  
pp. 442-447 ◽  
Author(s):  
Takao Minami ◽  
Michio Ogawa ◽  
Tsuyoshi Sugimoto ◽  
Kikushi Katsurada
Keyword(s):  
Brain Death ◽  
Oxygen Content ◽  
Clinical Status ◽  
Venous Blood ◽  
Common Finding ◽  
Mixed Venous Blood ◽  
Content Type ◽  
The Brain ◽  
Death Group ◽  
Mixed Venous

✓ The oxygen tension and acid-base values of internal jugular venous blood were compared to those of arterial and systemic mixed venous blood in 40 patients suffering from severe head injury. The results were divided into “brain death” and “coma groups” according to the clinical status when the sample was obtained. Hyperoxia of the jugular venous blood was a common finding in both groups, especially in the brain death group. The mean value of the arteriojugular venous oxygen content difference was 1.86 vol % in the brain death group, and 4.41 vol % in the coma group. Although most of the oxygen content differences in the brain death group were below 3 vol %, there was an overlap with the coma group at the low level of arteriojugular O2 difference. For definitive assessment of brain death, the fact that jugular pO2 was higher than that in systemic mixed venous pO2 was more valuable than the decrease of arteriojugular oxygen difference. The extreme hyperoxia of the jugular venous blood is possibly a sign of brain death, but should not be interpreted as the result of decreased oxygen consumption in the brain, because most of the jugular venous blood is returned from the extracerebral tissues. The causes of jugular hyperoxia in the state of brain death are discussed.

scholarly journals Hyperammonaemia does not impair brain function in the absence of net glutamine synthesis

1991 ◽  
Vol 277 (3) ◽  
pp. 697-703 ◽  
Author(s):  
R A Hawkins ◽  
J Jessy
Keyword(s):  
Amino Acids ◽  
Brain Function ◽  
Aromatic Amino Acids ◽  
Preceding Paper ◽  
Glucose Consumption ◽  
High Energy ◽  
High Energy Phosphates ◽  
Intermediary Metabolites ◽  
Glutamine Synthesis ◽  
The Brain

1. It has been established that chronic hyperammonaemia, whether caused by portacaval shunting or other means, leads to a variety of metabolic changes, including a depression in the cerebral metabolic rate of glucose (CMRGlc) increased permeability of the blood-brain barrier to neutral amino acids, and an increase in the brain content of aromatic amino acids. The preceding paper [Jessy, DeJoseph & Hawkins (1991) Biochem. J. 277, 693-696] showed that the depression in CMRGlc caused by hyperammonaemia correlated more closely with glutamine, a metabolite of ammonia, than with ammonia itself. This suggested that ammonia (NH3 and NH4+) was without effect. The present experiments address the question whether ammonia, in the absence of net glutamine synthesis, induces any of the metabolic symptoms of cerebral dysfunction associated with hyperammonaemia. 2. Small doses of methionine sulphoximine, an inhibitor of glutamine synthetase, were used to raise the plasma ammonia levels of normal rats without increasing the brain glutamine content. These hyperammonaemic rats, with plasma and brain ammonia levels equivalent to those known to depress brain function, behaved normally over 48 h. There was no depression of cerebral energy metabolism (i.e. the rate of glucose consumption). Contents of key intermediary metabolites and high-energy phosphates were normal. Neutral amino acid transport (tryptophan and leucine) and the brain contents of aromatic amino acids were unchanged. 3. The data suggest that ammonia is without effect at concentrations less than 1 mumol/ml if it is not converted into glutamine. The deleterious effect of chronic hyperammonaemia seems to begin with the synthesis of glutamine.

Myoglobin function and energy metabolism of isolated cardiac myocytes: effect of sodium nitrite

1991 ◽  
Vol 261 (4) ◽  
pp. 1-1
Author(s):  
Jeannette E. Doeller ◽  
Beatrice A. Wittenberg
Keyword(s):  
New York ◽  
Energy Metabolism ◽  
Cardiac Myocytes ◽  
Sodium Nitrite ◽  
Isolated Heart ◽  
High Energy ◽  
Heart Cells ◽  
High Energy Phosphates ◽  
Adult Rats ◽  
Isolated Cardiac Myocytes

Pages H53–H62, 1991: Jeannette E. Doeller and Beatrice A. Wittenberg. “Myoglobin function and energy metabolism of isolated cardiac myocytes: effect of sodium nitrite.” We regret that the following references were inadvertently dropped during printing. 26. Wittenberg, B. A., J. E. Doeller, R. K. Gupta, and R. L. White. Measurement of sarcolemmal permeability and intracellular pH, free magnesium, and high energy phosphates of isolated heart cells. In: Biology of Isolated Adult Cardiac Myocytes, edited by W. A. Clark, R. S. Decker, and T. K. Borg. New York: Elsevier, 1988, p. 188–130. 27. Wittenberg, B. A., and T. F. Robinson. Oxygen requirements, morphology, cell coat and membrane permeability of calcium tolerant myocytes from hearts of adult rats. Cell Tissue Res. 216: 231–251, 1981. 28. Wittenberg, B. A., and J. B. Wittenberg. Oxygen pressure gradients in isolated cardiac myocytes. J. Biol. Chem. 260: 6548–6554, 1985. 29. Wittenberg, B. A., and J. B. Wittenberg. Myoglobin-mediated oxygen delivery to mitochondria of isolated cardiac myocytes. Proc. Natl. Acad. Sci. USA 84: 7503–7607, 1987. 30. Wittenberg, B. A., and J. B. Wittenberg. Transport of oxygen in muscle. Annu. Rev. Physiol. 51: 857–878, 1989. 31. Wittenberg, B. A., J. B. Wittenberg, and P. R. B. Caldwell. Role of myoglobin in the oxygen supply to red skeletal muscle. J. Biol. Chem. 250: 9038–9043, 1975. 32. Wittenberg, J. B., and B. A. Wittenberg. Preparation of myoglobins. In: Methods of Enzymology, edited by S. P. Colowick and N. O. Kaplan. New York: Academic, 1981, vol. 76, p. 29–42. 33. Wittenberg, J. B., and B. A. Wittenberg. Mechanisms of cytoplasmic hemoglobin and myoglobin function. Annu. Reu. Biophys. Biophys. Chem. 19: 217–241, 1990.

Effect of hyperventilation on dynamics of cerebral energy metabolism

1975 ◽  
Vol 228 (6) ◽  
pp. 1862-1867 ◽  
Author(s):  
K Kogure ◽  
R Busto ◽  
A Matsumoto ◽  
P Scheinberg ◽  
OM Reinmuth
Keyword(s):  
Energy Metabolism ◽  
Closed System ◽  
Energy Production ◽  
Energy Charge ◽  
High Energy ◽  
Utilization Rate ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Cerebral Energy Metabolism ◽  
Extreme Degree

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA.Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.

scholarly journals Dissociated Expression of Mitochondrial and Cytosolic Creatine Kinases in the Human Brain: A New Perspective on the Role of Creatine in Brain Energy Metabolism

2013 ◽  
Vol 33 (8) ◽  
pp. 1295-1306 ◽  
Author(s):  
Matthew TJ Lowe ◽  
Eric H Kim ◽  
Richard LM Faull ◽  
David L Christie ◽  
Henry J Waldvogel
Keyword(s):  
Energy Metabolism ◽  
Human Brain ◽  
High Energy ◽  
Cellular Energy ◽  
Neuronal Populations ◽  
Neurologic Function ◽  
New Perspective ◽  
The Brain ◽  
Brain Energy

The phosphocreatine/creatine kinase (PCr/CK) system in the brain is defined by the expression of two CK isozymes: the cytosolic brain-type CK (BCK) and the ubiquitous mitochondrial CK (uMtCK). The system plays an important role in supporting cellular energy metabolism by buffering adenosine triphosphate (ATP) consumption and improving the flux of high-energy phosphoryls around the cell. This system is well defined in muscle tissue, but there have been few detailed studies of this system in the brain, especially in humans. Creatine is known to be important for neurologic function, and its loss from the brain during development can lead to mental retardation. This study provides the first detailed immunohistochemical study of the expression pattern of BCK and uMtCK in the human brain. A strikingly dissociated pattern of expression was found: uMtCK was found to be ubiquitously and exclusively expressed in neuronal populations, whereas BCK was dominantly expressed in astrocytes, with a low and selective expression in neurons. This pattern indicates that the two CK isozymes are not widely coexpressed in the human brain, but rather are selectively expressed depending on the cell type. These results suggest that the brain cells may use only certain properties of the PCr/CK system depending on their energetic requirements.

Abstract 289: Relationship Between Myocardial Glycogen Concentrations and Amplitude Spectrum Area During Ventricular Fibrillation in a Rat Model of Cardiac Arrest and Resuscitation

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Qiaohua Hu ◽  
Xiangshao Fang ◽  
Zhengfei Yang ◽  
Wanchun Tang
Keyword(s):  
Cardiac Arrest ◽  
Energy Metabolism ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Glycogen Content ◽  
Amplitude Spectrum ◽  
High Energy ◽  
Myocardial Energy Metabolism ◽  
Spectrum Area ◽  
The Relationship

Introduction: Myocardial high-energy phosphate (ATP) levels has been demonstrated correlating with amplitude spectrum area (AMSA) during ventricular fibrillation (VF) in previous experimental studies. In the present study, we investigated the relationship between AMSA and myocardial glycogen content (MGC),which can be used to reflect the status of myocardial energy metabolism indirectly during VF. Hypothesis: AMSA has a significantly correlation with MGC during VF in a rat model of cardiac arrest and resuscitation. Methods: Twenty male Sprague-Dawley rats weighing 350 to 450 g were utilized and randomized into two groups: VF and cardiopulmonary resuscitation (CPR) (VF/CPR group) or untreated VF (VF group). 5 mins of CPR was performed after 10 mins of untreated VF in VF/CPR animals. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 mins were calculated from ECG signals. The rats’ hearts were quickly removed at the predetermined time of 15 min for determines the glycogen contents by the anthrone reagent method using a glycogen assay kit. Results: AMSA values significantly decreased during untreated VF in both VF and VF/CPR animals. However, much greater AMSA during CPR was achieved by the VF/CPR group in comparison with the VF group. There was a marked and negative relationship between AMSA at VF 15 min and MGC. (Figure). Conclusion: MGC was significantly and negatively correlated with AMSA during VF in this rat model of cardiac arrest and resuscitation. In clinical practice, we can use AMSA to reflect the state of myocardial energy metabolism indirectly. Figure The changes of AMSA and relationship between AMSA and glycogen content:(A) The change of AMSA between VF/CRP group and VF group;(B) The relationship between AMSA and glycogen content. AMSA, amplitude spectrum area; V, time of ventricular fibrillation; # p <0.05 vs. V4.

scholarly journals Effects of Calcium Entry Blocker Emopamil on Postischemic Energy Metabolism of the Isolated Perfused Rat Brain

1987 ◽  
Vol 7 (4) ◽  
pp. 489-496 ◽  
Author(s):  
Gerhard Wilhelm Bielenberg ◽  
Heinz Haubruck ◽  
Josef Krieglstein
Keyword(s):  
Energy Metabolism ◽  
Flow Rate ◽  
Constant Pressure ◽  
High Energy ◽  
Calcium Entry ◽  
High Energy Phosphates ◽  
Calcium Entry Blocker ◽  
Constant Flow ◽  
Constant Flow Rate ◽  
Entry Blocker

The effects of emopamil on postischemic energy metabolism and electroencephalographic (EEG) recovery were investigated in the isolated rat brain perfused at either constant pressure or, alternatively, at constant flow rate. Flow rate and perfusion pressure were monitored continuously. The brains were perfused with a fluorocarbon emulsion for 30 min, and after 30 min of ischemia, perfusion was reinstituted for 5, 30, or 60 min. Global cerebral perfusion rate was increased by emopamil throughout the perfusion period and, accordingly, in brains perfused at a constant flow rate, perfusion pressure was reduced by the drug. At constant pressure perfusion, after 5 min after ischemia, cortical levels of creatine-phosphate, adenosine triphosphate (ATR), glucose, glucose-6-phosphate, and fructose-6-phosphate were higher in emopamil-treated brains than in controls, although the levels of adenosine diphosphate (ADP) and adenosine monophosphate (AMP) were reduced. When brains were perfused at constant flow rate, however, emopamil exhibited no effect on brain energy metabolism in the early reperfusion period. Postischemic restoration of high-energy phosphates proved to depend on the flow rate used. After 30 min of postischemic reperfusion, cortical levels of lactate were lower in emopamil-treated brains compared to controls at both constant pressure and constant volume perfusion. Postischemic lactate levels were independent of flow rate and were also reduced when emopamil was only present during reperfusion. The postischemic restoration of cortical EEG activity was improved by the calcium entry blocker. The results suggest that the restoration of high-energy phosphates during the early postischemic recovery can be mainly attributed to the vascular effect of emopamil, whereas the lower lactate levels are caused by a direct action of the calcium entry blocker on brain parenchyma.

Uremic encephalopathy: role of brain energy metabolism

1984 ◽  
Vol 247 (3) ◽  
pp. F527-F532
Author(s):  
C. A. Mahoney ◽  
P. Sarnacki ◽  
A. I. Arieff
Keyword(s):  
Renal Failure ◽  
Redox State ◽  
Adenine Nucleotide ◽  
Energy Charge ◽  
High Energy ◽  
Normal Brain ◽  
High Energy Phosphates ◽  
Adenine Nucleotide Pool ◽  
The Brain ◽  
Brain Energy

Uremia is associated with decreased brain oxygen consumption in humans and with decreased brain energy consumption in rodent models of acute renal failure. We measured the levels of high-energy phosphates and glycolytic intermediates in the brain of dogs with acute or chronic renal failure. We used methods of rapid brain tissue fixation that trap these labile metabolites at their in vivo levels. Creatine phosphate, ATP, and glucose were normal in the brain of animals with renal failure, indicating a normal brain energy reserve. The brain energy charge, which is the fraction of the total adenine nucleotide pool that contains high-energy phosphates, (ATP + 1/2ADP)/(ATP + ADP + AMP), was also normal despite an 8% decrease in the total adenine nucleotide pool. Mild hypoxia failed to alter the level of any of these metabolites. The brain redox state, (NAD+)/(NADH), was normal to high in acute renal failure, suggesting that oxygen supply was not limiting oxygen consumption. In the face of normal brain energy reserves, energy charge, and redox state, the decreased energy consumption of uremic brain probably results from decreased demand rather than limited supply.

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