Metabolic response to halothane in piglets susceptible to malignant hyperthermia: an in vivo 31P-NMR study

1993 ◽  
Vol 75 (2) ◽  
pp. 955-962 ◽  
Author(s):  
C. Decanniere ◽  
P. Van Hecke ◽  
F. Vanstapel ◽  
H. Ville ◽  
R. Geers
Keyword(s):  
Malignant Hyperthermia ◽  
Intracellular Ph ◽  
Metabolic Response ◽  
Stress Test ◽  
Recovery Period ◽  
Muscle Metabolism ◽  
Resonance Spectroscopy ◽  
Intracellular Acidosis ◽  
Nmr Study

Using in vivo 31P-nuclear magnetic resonance spectroscopy, we studied the skeletal muscle metabolism of 17 anesthetized malignant hyperthermia-susceptible piglets and 25 control piglets during and after a halothane stress test. At rest, the phosphocreatine- (PCr) to-ATP ratio was 12% higher in the anesthetized piglets than in the control piglets, which may reflect a higher proportion of fast glycolytic fibers in the former. About 15 min of halothane administration sufficed to provoke onset of a reaction, which was characterized by a reciprocal drop in PCr and an increase in Pi with commencing intracellular acidosis. Halothane was withdrawn after a 20% drop in PCr. Within the next few minutes, intracellular pH dropped sharply and phosphomonoesters (PME) accumulated excessively. ATP was observed to decrease in 8 of the 17 animals. Halothane inhalation provoked a switch of metabolism toward glycolysis. Accumulation of PME suggests a mismatch between glycogenolysis and glycolysis. Despite severe acidification, glycolysis was not completely halted. Recovery of PCr and Pi started approximately 5 min after halothane withdrawal, with a longer time constant for recovery of the former. PME and intracellular pH aberrations lingered and started to recover later. Lost ATP was never restored within the observed recovery period of approximately 20 min.

Effect of insulin on intracellular pH and phosphate metabolism in human skeletal muscle in vivo

1991 ◽  
Vol 81 (1) ◽  
pp. 123-128 ◽  
Author(s):  
D. J. Taylor ◽  
S. W. Coppack ◽  
T. A. D. Cadoux-Hudson ◽  
G. J. Kemp ◽  
G. K. Radda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Inorganic Phosphate ◽  
Human Skeletal Muscle ◽  
Muscle Metabolism ◽  
Normal Subjects ◽  
Phosphate Concentration ◽  
Resonance Spectroscopy ◽  
Phosphorus Containing

1. 31P nuclear magnetic resonance spectroscopy and the hyperinsulinaemic-euglycaemic clamp were used simultaneously to assess the effect of insulin on intracellular pH and the major phosphorus-containing metabolites of normal human skeletal muscle in vivo in four normal subjects. 2. Insulin and glucose were infused for 120 min. Plasma insulin increased approximately 10-fold over pre-clamp levels (5.6 ± 0.9 m-units/l pre-clamp and 54 ± 5 m-units/l over the last hour of infusion; mean ± sem, n = 4). Plasma glucose concentration did not change significantly (5.4 ± 0.2 mmol/l pre-clamp and 5.5 ± 0.1 mmol/l over the last hour of infusion). 3. Insulin and glucose infusion resulted in a decline in the intracellular pH of forearm muscle of 0.027 ± 0.007 unit/h (P < 0.01), whereas in control studies of the same subjects, pH rose by 0.046 ± 0.005 unit/h (P < 0.001). 4. In the clamp studies, intracellular inorganic phosphate concentration rose by 18%/h, whereas ATP, phosphocreatine and phosphomonoester concentrations did not change. In plasma, inorganic phosphate concentration was 1.16 ± 0.05 mmol/l before infusion, and this decreased by a mean rate of 0.14 mmol h−1 l−1. No change was observed in any of these intracellular metabolites in the control studies. 5. The results show that, under physiological conditions, insulin does not raise intracellular pH in human muscle, and thus cannot influence muscle metabolism by this mechanism. The results also suggest that insulin causes a primary increase in the next flux of inorganic phosphate across the muscle cell membrane.

Muscle metabolism during exercise in young and older untrained and endurance-trained men

1993 ◽  
Vol 75 (5) ◽  
pp. 2125-2133 ◽  
Author(s):  
A. R. Coggan ◽  
A. M. Abduljalil ◽  
S. C. Swanson ◽  
M. S. Earle ◽  
J. W. Farris ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Muscle Mass ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
Plantar Flexion ◽  
Muscle Metabolism ◽  
Resonance Spectroscopy ◽  
Age Related ◽  
Rate Of Increase ◽  
Response To Exercise

To examine effects of aging and endurance training on human muscle metabolism during exercise, 31P magnetic resonance spectroscopy was used to study the metabolic response to exercise in young (21–33 yr) and older (58–68 yr) untrained and endurance-trained men (n = 6/group). Subjects performed graded plantar flexion exercise with the right leg, with metabolic responses measured using a 31P surface coil placed over the lateral head of the gastrocnemius muscle. Muscle biopsy samples were also obtained for determination of citrate synthase activity. Rate of increase in P(i)-to-phosphocreatine ratio with increasing power output was greater (P < 0.01) in older untrained [0.058 +/- 0.022 (SD) W-1] and trained men (0.042 +/- 0.010 W-1) than in young untrained (0.038 +/- 0.017 W-1) and trained men (0.024 +/- 0.010 W-1). Plantar flexor muscle cross-sectional area and volume (determined using 1H magnetic resonance imaging) were 11–12% (P < 0.05) and 16–18% (P < 0.01) smaller, respectively, in older men. When corrected for this difference in muscle mass, age-related differences in metabolic response to exercise were reduced by approximately 50% but remained significant (P < 0.05). Citrate synthase activity was approximately 20% lower (P < 0.001) in older untrained and trained men than in corresponding young groups and was inversely related to P(i)-phosphocreatine slope (r = -0.63, P < 0.001). Age-related reductions in exercise capacity were associated with an altered muscle metabolic response to exercise, which appeared to be due to smaller muscle mass and lower muscle respiratory capacity of older subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Skeletal muscle metabolism and work capacity: a 31P-NMR study of Andean natives and lowlanders

1991 ◽  
Vol 70 (5) ◽  
pp. 1963-1976 ◽  
Author(s):  
G. O. Matheson ◽  
P. S. Allen ◽  
D. C. Ellinger ◽  
C. C. Hanstock ◽  
D. Gheorghiu ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Muscle Metabolism ◽  
Work Capacity ◽  
Calf Muscle ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Muscle Work ◽  
Nmr Study ◽  
Nuclear Magnetic

Two metabolic features of altitude-adapted humans are the maximal O2 consumption (VO2max) paradox (higher work rates following acclimatization without increases in VO2max) and the lactate paradox (progressive reductions in muscle and blood lactate with exercise at increasing altitude). To assess underlying mechanisms, we studied six Andean Quechua Indians in La Raya, Peru (4,200 m) and at low altitude (less than 700 m) immediately upon arrival in Canada. The experimental strategy compared whole-body performance tests and single (calf) muscle work capacities in the Andeans with those in groups of sedentary, power-trained, and endurance-trained lowlanders. We used 31P nuclear magnetic resonance spectroscopy to monitor noninvasively changes in concentrations of phosphocreatine [( PCr]), [Pi], [ATP], [PCr]/[PCr] + creatine ([Cr]), [Pi]/[PCr] + [Cr], and pH in the gastrocnemius muscle of subjects exercising to fatigue. Our results indicate that the Andeans 1) are phenotypically unique with respect to measures of anaerobic and aerobic work capacity, 2) despite significantly lower anaerobic capacities, are capable of calf muscle work rates equal to those of highly trained power- and endurance-trained athletes, and 3) compared with endurance-trained athletes with significantly higher VO2max values and power-trained athletes with similar VO2max values, display, respectively, similar and reduced perturbation of all parameters related to the phosphorylation potential and to measurements of [Pi], [PCr], [ATP], and muscle pH derivable from nuclear magnetic resonance. Because the lactate paradox may be explained on the basis of tighter ATP demand-supplying coupling, we postulate that a similar mechanism may explain 1) the high calf muscle work capacities in the Andeans relative to measures of whole-body work capacity, 2) the VO2max paradox, and 3) anecdotal reports of exceptional work capacities in indigenous altitude natives.

Influence of intracellular acidosis on contractile function in the working rat heart

1987 ◽  
Vol 253 (6) ◽  
pp. H1499-H1505 ◽  
Author(s):  
F. M. Jeffrey ◽  
C. R. Malloy ◽  
G. K. Radda
Keyword(s):  
Stroke Volume ◽  
Intracellular Ph ◽  
Rat Heart ◽  
Contractile Function ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Intracellular Acidosis ◽  
Tension Development ◽  
O2 Delivery

The decrease in myocardial contractility during ischemia, hypoxia, and extracellular acidosis has been attributed to intracellular acidosis. Previous studies of the relationship between pH and contractile state have utilized respiratory or metabolic acidosis to alter intracellular pH. We developed a model in the working perfused rat heart to study the effects of intracellular acidosis with normal external pH and optimal O2 delivery. Intracellular pH and high-energy phosphates were monitored by 31P nuclear magnetic resonance spectroscopy. Hearts were perfused to a steady state with a medium containing 10 mM NH4Cl (extracellular pH, 7.4). The subsequent washout of NH3 from the cytosol generated a slight acidosis (from intracellular pH 7.0 to 6.8) which was associated with little change in the determinants of O2 consumption (rate-pressure product) and O2 delivery (coronary flow). Acidosis induced a substantial decrease in aortic flow and stroke volume which was associated with little change in peak systolic pressure. Results were qualitatively similar at different external [Ca2+] (1.75, 2.5, 3.15 mM) and preload (12 or 21 cmH2O) but were most prominent at the lowest external [Ca2+] and left atrial pressure. In contrast to this model of isolated intracellular acidosis, hearts subject to a respiratory (extracellular plus intracellular) acidosis showed a marked reduction in pressure development. It was concluded that 1) for the same intracellular acidosis the influence on tension development was more pronounced with a combined extra- and intracellular acidosis than with an isolated intracellular acidosis, and 2) stroke volume at constant preload was impaired by intracellular acidosis even though changes in developed pressure were minimal. These observations suggest that isolated intracellular acidosis has adverse effects on diastolic compliance and/or relaxation.

scholarly journals Measurement of the acute metabolic response to hypoxia in rat tumours in vivo using magnetic resonance spectroscopy and hyperpolarised pyruvate

2015 ◽  
Vol 116 (3) ◽  
pp. 392-399 ◽  
Author(s):  
Joanne E. Bluff ◽  
Steven Reynolds ◽  
Stephen Metcalf ◽  
Tooba Alizadeh ◽  
Samira M. Kazan ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Metabolic Response ◽  
Resonance Spectroscopy

Diaphragmatic fatigue assessed by 31P-magnetic resonance spectroscopy in vivo

1993 ◽  
Vol 264 (5) ◽  
pp. C1111-C1118 ◽  
Author(s):  
D. G. Nichols ◽  
J. R. Buck ◽  
S. M. Eleff ◽  
D. C. Shungu ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Intracellular Ph ◽  
Oxidative Metabolism ◽  
Compound Action Potential ◽  
Separate Group ◽  
Resonance Spectroscopy ◽  
Transdiaphragmatic Pressure ◽  
Control Value

We tested whether fatigue of the piglet diaphragm is associated with inadequate oxidative metabolism as measured by magnetic resonance spectroscopy (MRS). An MRS measured ratio of inorganic phosphate to phosphocreatine (Pi/PCr) > or = 1 was taken as evidence of inadequate oxidative metabolism. Piglets (n = 10) underwent phrenic nerve pacing for 90 min with stimulation frequency of 30 Hz and duty cycle of 0.33. In a separate group of six piglets PCr, Pi, ATP, and intracellular pH were measured by in vivo MRS, and diaphragmatic blood flow was measured with radioactive microspheres at control, 2, 10, 45, 60, and 90 min of pacing. Transdiaphragmatic pressure fell from 25 +/- 3 to 15 +/- 2 mmHg (61 +/- 5%) at 2 min and remained depressed in a separate group of four piglets (P < 0.05). Conversely, compound action potential amplitude remained constant for the first 10 min of pacing and fell to 68 +/- 5% of control at 45 min (P < 0.05). Pi/PCr rose from a control value of 0.32 +/- 0.06 to 0.92 +/- 0.23 at 2 min and 0.79 +/- 0.03 at 10 min (P < 0.05) before returning toward control at 45-90 min. O2 delivery increased from 4.6 +/- 1.2 to 24.7 +/- 4.8 ml.min-1.100 g-1 at 2 min and 18.4 +/- 2.2 ml.min-1.100 g-1 at 10 min (P < 0.05) but then fell to lower levels at 45-90 min. ATP and intracellular pH remained constant except for a decline in pH to 6.98 +/- 0.09 at 45 min (P < 0.05) from the control value of 7.26 +/- 0.06.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuronal pH Regulation: Constant Normal Intracellular pH is Maintained in Brain during Low Extracellular pH Induced by Acetazolamide—31P NMR Study

1989 ◽  
Vol 9 (3) ◽  
pp. 417-421 ◽  
Author(s):  
Sissel Vorstrup ◽  
Karl Erik Jensen ◽  
Carsten Thomsen ◽  
Ole Henriksen ◽  
Niels A. Lassen ◽  
...  
Keyword(s):  
Intracellular Ph ◽  
Ph Regulation ◽  
Extracellular Ph ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Nmr Study ◽  
Resonance Frequencies ◽  
The Mean ◽  
Ph Decrease ◽  
Body Scanner

The intracellular pH in the brain was studied in six healthy volunteers before and immediately after the administration of 2 g of acetazolamide. Phosphorus-31 nuclear magnetic resonance spectroscopy by a 1.5 tesla whole-body scanner was used. The chemical shift between the inorganic phosphate and the phosphocreatine resonance frequencies was used for indirect assessment of the intracellular pH. The mean baseline intracellular pH was 7.05 ± 0.04 (SD). The mean pH changes obtained at 15-min intervals within the first hour of acetazolamide administration were −0.03 ± 0.04 (SD), −0.02 ± 0.03 (SD), and 0.00 ± 0.04 (SD), i.e., no statistically significant pH decrease was observed during the period where extracellular pH is known to drop markedly. Although several factors contribute to the lack of change of the intraneuronal pH, we will discuss that this observation in addition might suggest a direct intracerebral effect of acetazolamide.

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