scholarly journals Effects of Hypoxic Hypoxia on Cerebral Phosphate Metabolites and pH in the Anesthetized Infant Rabbit

1985 ◽  
Vol 5 (4) ◽  
pp. 512-516 ◽  
Author(s):  
Ricardo González-Méndez ◽  
Ann McNeill ◽  
George A. Gregory ◽  
Susan D. Wall ◽  
Charles A. Gooding ◽  
...  
Keyword(s):  
High Energy ◽  
Hypoxic Hypoxia ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Arterial Blood ◽  
A Value ◽  
Venous Infusion ◽  
The Brain

The effects of hypoxic hypoxia on high-energy phosphate metabolites and intracellular pH (pHi) in the brain of the anesthetized infant rabbit were studied in vivo using 31P nuclear magnetic resonance spectroscopy. Five 10- to 16-day-old rabbits were anesthetized with 1.5% halothane. Ventilation was controlled to maintain normocarbia. Inspired O2 fraction was adjusted to produce three states of arterial oxygenation: hyperoxia (Pao2 > 250 mm Hg), normoxia (Pao2 ∼ 100 mm Hg), and hypoxia (Pao2 25–30 mm Hg). During hypoxia, blood pressure was kept within 20% of control values with a venous infusion of epinephrine. During hyperoxia, the phosphocreatine-to-ATP ratio was 0.86, a value that is 2–2.5 times less than that reported for adults. During normoxia, ATP decreased by 20% and Pi increased by 90% from hyperoxia values. During 60 min of hypoxia, the concentrations of high-energy phosphate metabolites did not change, but intracellular and arterial blood pH (pHa) decreased significantly. When hyperoxia was reestablished, pHi returned to normal and pHa remained low. These results suggest that during periods of hypoxemia, the normotensive infant rabbit maintains intracellular concentrations of cerebral high-energy phosphates better than has been reported for adult animals.

The effects of hypovolemic hypotension on high-energy phosphate metabolism of traumatized brain in rats

1988 ◽  
Vol 68 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Naoki Ishige ◽  
Lawrence H. Pitts ◽  
Isabelle Berry ◽  
Merry C. Nishimura ◽  
Thomas L. James
Keyword(s):  
High Energy ◽  
High Energy Phosphates ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
Content Type ◽  
Arterial Blood ◽  
High Energy Phosphate Metabolism ◽  
Impact Injury ◽  
Hypovolemic Hypotension

✓ To clarify the effect of hypovolemic hypotension on high-energy phosphate metabolism in head injury, sequential changes in in vivo phosphorus-31 magnetic resonance (31P MR) spectra were compared in 35 rats after impact injury with and without hypotension. Fourteen rats were subjected to hypotension alone (mean arterial blood pressure (MABP) of either 40 or 30 mm Hg for 60 minutes), seven to fluid-percussion impact injury (4 to 5 atm) alone, and 14 to impact injury and hypotension (MABP of 40 to 30 mm Hg). Impact injury alone caused a transient decrease in the phosphocreatine (PCr) level and an increase in the inorganic phosphate (Pi) value. While hypotension alone produced only small changes on 31P MR spectra, impact injury plus hypotension caused pronounced changes. Impact injury and an MABP of 40 mm Hg caused a 50% decrease in PCr concentration and an approximately twofold increase in Pi level, which were significantly greater than values in rats with impact injury alone. Impact injury and an MABP of 30 mm Hg also caused a significant decrease in adenosine triphosphate value, which was not observed in rats with impact injury alone or with an MABP of 30 mm Hg alone. Decreases in intracellular pH were greater in rats with impact injury and hypotension. After traumatic injury, the brain is extremely vulnerable to hypovolemic hypotension, as reflected in the loss of high-energy phosphates in brain.

Effects of hypercapnia on ECoG and oxidative metabolism in neonatal dog brain

1995 ◽  
Vol 78 (6) ◽  
pp. 2272-2278 ◽  
Author(s):  
H. Yoshioka ◽  
H. Miyake ◽  
D. S. Smith ◽  
B. Chance ◽  
T. Sawada ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Resonance Spectroscopy ◽  
Respiratory Enzymes ◽  
Arterial Pco2 ◽  
A Value ◽  
Electrocorticogram Ecog ◽  
The Brain ◽  
Mitochondrial Respiratory

The effects of hypercapnia on cerebral electrical activity and mitochondrial oxidative phosphorylation were studied in the anesthetized neonatal dog by using the electrocorticogram (ECoG) and 31P-magnetic resonance spectroscopy. Three levels of hypercapnia with arterial PCO2 values of approximately 70, 100, and 140 Torr reduced the intracellular pH of the brain from 7.11 to 6.99, 6.87, and 6.76, respectively. These levels of hypercapnia also reduced ADP concentration ([ADP]) from 21.5 to 18.1, 14.8, and 12.9 microM as well as the average ECoG power output by 20, 30, and 40%. A Michaelis-Menten relationship for the mitochondrial respiratory enzymes was fitted with [ADP] and the change in the average ECoG. The result suggests that mitochondrial respiration is regulated by [ADP] and that the in vivo Michaelis-Menten constant for ADP was 21 microM, a value close to the in vitro value. The mitochondrial maximal reaction velocity was reduced by only 10% during hypercapnia and showed no relationship with the degree of acidosis, suggesting that mitochondrial respiratory enzymes are not responsible for the inhibition of the brain electrical activity.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans

2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Underlying Mechanism ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
High Energy Phosphate ◽  
Available Energy ◽  
Healthy Humans ◽  
High Energy Phosphate Metabolism ◽  
The Brain

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

scholarly journals In vivo Magnetic Resonance Spectroscopy and its Application to Neuropsychiatric Disorders

2002 ◽  
Vol 47 (4) ◽  
pp. 315-326 ◽  
Author(s):  
Jeffrey A Stanley
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Early Stage ◽  
Neuropsychiatric Disorders ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Membrane Phospholipids ◽  
High Energy Phosphate ◽  
Spectroscopy Studies

In vivo magnetic resonance spectroscopy (MRS) is the only noninvasive imaging technique that can directly assess the living biochemistry in localized brain regions. In the past decade, spectroscopy studies have shown biochemical alterations in various neuropsychiatric disorders. These first-generation studies have, in most cases, been exploratory but have provided insightful biochemical information that has furthered our understanding of different brain disorders. This review provides a brief description of spectroscopy, followed by a literature review of key spectroscopy findings in schizophrenia, affective disorders, and autism. In schizophrenia, phosphorus spectroscopy studies have shown altered metabolism of membrane phospholipids (MPL) during the early course of the illness, which is consistent with a neurodevelopmental abnormality around the critical period of adolescence when the illness typically begins. Children and adolescents who are at increased genetic risk for schizophrenia show similar MPL alterations, suggesting that schizophrenia subjects with a genetic predisposition may have a premorbid neurodevelopmental abnormality. Independent of medication status, bipolar subjects in the depressive state tended to have higher MPL precursor levels and a deficit of high-energy phosphate metabolites, which also is consistent with major depression, though these results varied. Further bipolar studies are needed to investigate alterations at the early stage. Lastly, associations between prefrontal metabolism of high-energy phosphate and MPL and neuropsychological performance and reduced N-acetylaspartate in the temporal and cerebellum regions have been reported in individuals with autism. These findings are consistent with developmental alterations in the temporal lobe and in the cerebellum of persons with autism. This paper discusses recent findings of new functions of N-acetylaspartate.

Myocardial high-energy phosphate metabolism is altered after treatment with anthracycline in childhood

2000 ◽  
Vol 10 (6) ◽  
pp. 610-617 ◽  
Author(s):  
Andrea B. Eidenschink ◽  
Gerrit Schröter ◽  
Stefan Müller-Weihrich ◽  
Heiko Stern
Keyword(s):  
Adenosine Triphosphate ◽  
High Energy ◽  
Left Ventricular ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
Resonance Spectroscopy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
High Energy Phosphate Metabolism

AbstractObjectivesWe aimed to investigate whether changes in high-energy phosphate metabolism after treatment of children and young adults with anthracycline can be demonstrated non-invasively by 31P magnetic resonance spectroscopy.BackgroundAbnormal myocardial energy metabolism has been suggested as a mechanism for anthracycline-induced cardiotoxicity. Deterioration in such has been shown in animal studies by resonance spectroscopy.MethodsWe studied 62 patients, with a mean age of 13.5 ±5 years,3.7±4.3 years after a cumulative anthracycline dose of 270±137 mg/m2. Normal echocardiographic findings had been elicited in 54 patients. The control group consisted of 28 healthy subjects aged 20±7 years. Resonance spectrums of the anterior left ventricular myocardium were obtained at 1.5 Tesla using an image-selected in vivo spectroscopy localization technique.ResultsThe ratio of phosphocreatine to adenosine triphosphate after blood correction was 1.09±0.43 for the patients, and 1.36±0.36 (mean±SD)for controls (p = 0.005), with a significantly reducedmean ratio even in the subgroup of patients with normal echocardiographic results ( l.11 ± 0. 44 versus1.36±0.36, p=0.01). The ratio did not correlate with the cumulative dose of anthracycline. The ratio of phosphodiester to adenosine triphosphate was similar in patients and controls (0.90±0.56 versus 0.88±0.62).ConclusionsIn patients treated with anthracyclines in childhood, myocardial high-energy phosphate metabolism may be impaired even in the absence of cardiomyopathy. Our data support the concept that anthracycline-induced cardiotoxicity is not clearly dose dependent.

High-energy phosphates and tension production in rabbit tibialis anterior/extensor digitorum longus muscles

1997 ◽  
Vol 82 (3) ◽  
pp. 1024-1024 ◽  
Author(s):  
T. W. Ryschon ◽  
J. C. Jarvis ◽  
S. Salmons ◽  
R. S. Balaban
Keyword(s):  
Tibialis Anterior ◽  
Extensor Digitorum Longus ◽  
Energy State ◽  
Oxidative Capacity ◽  
High Energy ◽  
Extensor Digitorum ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Control Muscle

Ryschon, T. W., J. C. Jarvis, S. Salmons, and R. S. Balaban.High-energy phosphates and tension production in rabbit tibialis anterior/extensor digitorum longus muscles. J. Appl. Physiol. 82(3): 1024–1029, 1997.—The effects of repetitive muscle contraction on energy state and tension production were studied in rabbit tibialis anterior/extensor digitorum longus muscles that had been subjected to 90 days of continuous indirect electrical stimulation at 10 Hz. Anesthetized chronically stimulated and control rabbits were challenged with 15 min of stimulation at 4 and 15 tetani/min. Pi-to-phosphocreatine (PCr) ratio (Pi/PCr) was measured in vivo before, during, and after acute stimulation by31P-magnetic resonance spectroscopy, and tension was recorded at the same time. Although Pi/PCr was low at rest, it was significantly higher in chronically stimulated muscle than in control muscle (0.20 ± 0.02 vs. 0.05 ± 0.01, P < 0.05). Stimulation of control muscle for 15 min at both 4 and 15 tetani/min induced a significant rise in Pi/PCr, whereas the same conditions in chronically stimulated muscle did not produce any significant departure from initial levels. The tension produced by control muscle fell to 93 ± 3% of its initial value during stimulation at 4 tetani/min and to 61 ± 7% at 15 tetani/min, respectively. In chronically stimulated muscle, on the other hand, tension was potentiated above its initial level at both stimulation rates (135 ± 15 and 138 ± 11%, respectively) and remained significantly elevated throughout each trial. The ability of chronically stimulated muscle to sustain high levels of activity with minimal perturbations in Pi/PCr or decrement in tension is attributable to cellular adaptations that include a well-documented increase in oxidative capacity.

Oxygen delivery does not limit cardiac performance during high work states

1999 ◽  
Vol 277 (1) ◽  
pp. H50-H57 ◽  
Author(s):  
Jianyi Zhang ◽  
Yo Murakami ◽  
Yi Zhang ◽  
Yong K Cho ◽  
Yun Ye ◽  
...  
Keyword(s):  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Creatine Phosphate ◽  
High Energy ◽  
Artery Occlusion ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Myocardial Oxygenation ◽  
High Work

This study tested the hypothesis that the loss of myocardial high-energy phosphates (HEP), which occurs during high cardiac work states [J. Zhang, D. J. Duncker, Y. Xu, Y. Zhang, G. Path, H. Merkle, K. Hendrich, A. H. L. From, R. Bache, and K. Uğurbil. Am. J. Physiol. 268: ( Heart Circ. Physiol. 37): H1891–H1905, 1995], is not the result of insufficient intracellular O2 availability. To evaluate the state of myocardial oxygenation, the proximal histidine signal of deoxymyoglobin (Mb-δ) was determined with1H nuclear magnetic resonance spectroscopy (MRS), whereas HEP were examined with31P MRS. Normal dogs ( n = 11) were studied under basal conditions and during combined infusion of dobutamine and dopamine (20 μg ⋅ kg−1 ⋅ min−1iv each), which increased rate-pressure products to >50,000 mmHg ⋅ beats ⋅ min−1. Creatine phosphate (CP) was expressed as CP/ATP, and myocardial myoglobin desaturation was normalized to the Mb-δ resonance present during total coronary artery occlusion. This Mb-δ resonance appeared at 71 parts per million downfield from the water resonance. CP/ATP decreased from 2.22 ± 0.12 during the basal state to 1.83 ± 0.09 during the high work state ( P < 0.01), whereas ΔPi/CP increased from 0 to 0.21 ± 0.04 ( P < 0.01). Despite these HEP changes, Mb-δ remained undetectable. In contrast, when a coronary stenosis was applied to produce a similar decrease in CP/ATP, Mb-δ reached 0.38 ± 0.10 of the value present during total coronary occlusion. These data demonstrate that Mb-δ is readily detected in vivo during limitation of coronary blood flow sufficient to cause a decrease of myocardial CP/ATP. However, similar HEP changes that occur at high work states in the absence of coronary occlusion are not associated with a detectable Mb-δ resonance. The findings support the hypothesis that the myocardial HEP changes observed at high work states are not due to inadequate O2 availability to the mitochondria and emphasize the limitations of interpreting HEP alterations in the absence of knowing the level of myocyte oxygenation.

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