PubMed Health⌕ Search

Biomedical subjects

F Brunotte

Publications and source records attributed to F Brunotte.

102 records · Page 6Linked to original sources
PubMed1983

67Ga and 59Fe uptake by tumor cells treated with hyperthermia or hyperthermia plus lanthanum.

The uptake of 67Ga-citrate and 59Fe-citrate by tumor cells treated with hyperthermia or with hyperthermia plus lanthanum has been studied. The comparison of these results with ion flux determinations (42K) appears to indicate that hyperthermia alone or combined with lanthanum modifies the ionic permeability of the plasma membrane. This phenomenon seems to be responsible for the increased accumulation of 67Ga and 59Fe.

Animals↗
PubMed1983

On the mechanisms of 67Ga and 59Fe uptake by tumors.

The uptake of 67Ga-citrate and 59Fe-citrate in the presence or absence of gallium and iron carriers, was studied on DS-sarcoma-bearing rats. Differences of uptake pattern were observed with both radionuclides. The tumor uptake of 67Ga is greatly affected by both carriers while 59Fe uptake is independent of the presence of carriers. The role of isotopic dilution, ionic competition, and the probable presence of high and low affinity binding sites in this phenomenon are discussed.

Animals↗
PubMed1982

Ionic competition and 67Ga in vivo accumulation.

The effect of several citrates of trivalent cations on 67Ga citrate uptake by tumor-bearing animals has been studied. A relationship between the ionic size of the simultaneously injected cation and the 67Ga uptake inhibition indicates that the cation characteristics (ionic radius and electrical charge) seem to play the most important role in this radioactivity accumulation. The apparent agreement of this phenomenon with the isomorphous replacement hypothesis is discussed.

Animals↗
PubMedDate not supplied

Relationship between increased peak oxygen uptake and modifications in skeletal muscle metabolism following rehabilitation after myocardial infarction.

PURPOSE: Rehabilitation after myocardial infarction produces an increased peak oxygen uptake (VO2peak). This study investigates the relationship between the modifications in skeletal muscle metabolism and the modification in VO2peak induced by a standard program of physical training following a myocardial infarction. METHODS: Seventeen patients (14 male, 3 female) were studied by phosphorus 31(31P) magnetic resonance spectroscopy after the acute phase of a myocardial infarction and after 2 months of rehabilitation. Changes in calf muscle pH, phosphocreatine, and inorganic phosphates were measured at rest and during a plantar flexion-type incremental workload protocol. Calf muscle pH, phosphocreatine/(phosphocreatine + inorganic phosphates), and inorganic phosphates/phosphocreatine ratios were compared at the highest identical workload attained in both studies. The VO2peak (mL/kg/min) was determined during a cycle stress test. RESULTS: At the highest identical workload attained in both tests, the ratio phosphocreatine/(phosphocreatine + inorganic phosphates) was significantly higher (0.48 +/- 0.15 to 0.57 +/- 0.18: P < .001), and the ratio inorganic phosphates/phosphocreatine was lower (1.38 +/- 1.14 to 0.99 +/- 0.87: P < .01). After rehabilitation, no difference was observed for the pH at stress (6.83 +/- 0.16 to 6.91 +/- 0.14: not significant [NS]). The increase in the VO2peak was significant after rehabilitation (24 +/- 9 to 29 +/- 11 mL/kg/min: P < .001). The VO2peak improvement induced by the physical training was correlated with the increase in the phosphocreatine/(phosphocreatine + inorganic phosphates) (r = 0.818, P < .001). CONCLUSIONS: The reduction in phosphocreatine depletion indicated that the oxidative capacity of the skeletal muscle was improved during the rehabilitation. The good correlation between the indexes of skeletal muscle metabolism and VO2peak suggests the peripheral effect of training.

Adaptation, Physiological↗
PubMedDate not supplied

Effects of low-frequency electrical stimulation of quadriceps and calf muscles in patients with chronic heart failure.

PURPOSE: The aim of this preliminary study was to evaluate the effects of low-frequency electrical stimulation of quadriceps and calf muscles on global exercise capacities, skeletal muscle metabolism, calf muscle volume, and cardiac output in patients with chronic heart failure. METHODS: Fourteen patients with chronic heart failure (mean age of 56.4 years +/- 9.1 SD; mean radionuclide left ventricular ejection fraction of 22.3% +/- 8.8 SD) underwent 5 weeks (1 hour per day, 5 days per week) of low-frequency electrical stimulation of quadriceps and calf muscles. RESULTS: Low-frequency electrical stimulation was well tolerated. Exercise capacity and the calf muscles volumes increased significantly after rehabilitation in comparison with prior rehabilitation (the peak oxygen consumption increased from 17.2 mL/(kgmin) +/- 5.3 SD to 19.6 mL/(kgmin) +/- 5.9 SD; the anaerobic threshold increased from 12.3 mL/(kgmin) +/- 3.2 SD to 15.2 mL/(kgmin) +/- 3.3 SD; the 6-minute walking test increased from 419 m +/- 122 SD to 459 m +/- 114.3 SD; the gastrocnemius volume increased from 259.4 cm3 +/- 58 SD to 273.4 cm3 +/- 74 SD, and the soleus volume increased from 319 cm3 +/- 42.9 SD to 338 cm3 +/- 52.5 SD). The New York Heart Association class was improved after rehabilitation. The P-31 nuclear magnetic resonance spectroscopy of gastrocnemius muscle data were not significantly modified after rehabilitation, thereby inferring that no significant improvement of the muscle metabolism occurred. These data reinforce the hypothesis of an increased muscle mass during stimulation. It is noteworthy that the electrical stimulation did not increase cardiac output at any stage; an enormous asset in favor of this mode of rehabilitation. CONCLUSION: These results suggest that low-frequency muscular electrical stimulation is well tolerated, induces an increased exercise capacity in patients with chronic heart failure, without an undesirable increase in cardiac output.

Cardiac Output↗
PubMedDate not supplied

Muscle metabolism assessed by phosphorus-31 nuclear magnetic resonance spectroscopy after myocardial infarction in rehabilitated patients: a 1-year follow-up.

BACKGROUND: The most common effect of postmyocardial infarction (post MI) rehabilitation is an increase of peak maximal oxygen consumption correlated with changes in calf muscle metabolism, but there are few data on follow-up after rehabilitation on skeletal muscle and maximal oxygen consumption. The purpose of this study was to investigate the respective modifications in skeletal muscle metabolism and peak oxygen consumption (VO2) occurring during a supervised rehabilitation program and 1 year after MI in patients free of heart failure. METHODS: Fifteen outpatients were studied prospectively after the acute phase of the MI, at the end of the rehabilitation program (2 months after the MI), and 1 year after. The rehabilitation comprised 20 sessions with three sessions per week. The program consisted of exercise training with bicycle, arm ergometer, and treadmill. The program also included respiratory exercises, psychological support, and counseling for secondary prevention of cardiovascular diseases. At each visit, a stress test on a bicycle ergometer was performed and the peak VO2 was measured. Phosphorus magnetic resonance spectroscopy of the gastrocnemius muscle was performed at rest and during a plantar flexion-type exercise against an adjustable load. Data were analyzed using analysis of variance and post-hoc test when appropriate. RESULTS: The mechanical power output measured during the bicycle exercise increased from 111 +/- 28 watts at the post MI test to 136 +/- 40 watts after rehabilitation (post rehab) and decreased to 125 +/- 36 watts at 1 year. The peak VO2 increased significantly (P < 0.05) from 22 +/- 7 ml/kg-1/min-1 (post MI) to 27 +/- 9 ml/kg-1/min-1 (post rehab), and decreased significantly to 24 +/- 8 ml/kg-1/min-1 (1 year). The mechanical power output measured in the magnet during the stress test increased from 2.22 +/- 0.13 watts (post MI) to 2.85 +/- 1.24 (post rehab), and stabilized at 2.78 +/- 1.10 watts at 1 year. At the highest workload attained in the three successive tests, the phosphocreatine/(phosphocreatine + inorganic phosphate) ratio rose significantly (P < 0.05) from 0.46 +/- 0.13 (post MI) to 0.51 +/- 0.13 (post rehab) and remained at 0.51 +/- 0.13 at 1 year. CONCLUSION: The improvement of the peak VO2 after training post MI is not maintained 1 year later. This decline is not accompanied by muscular metabolic abnormalities. This suggests that the muscle metabolism after MI remains normal, and that the long-term decrease of the peak VO2 reflects a global deconditioning that should be avoided by maintaining a long-term phase III rehabilitation program.

Adult↗
PubMedDate not supplied

[N-acetyl-aspartate abnormalities in internal-temporal epileptic foci using proton magnetic resonance spectroscopy].

The aim of this study was to characterize the neurochemical abnormalities related to N-acetyl-aspartate which is a neuronal marker, within an epilepticus focus located in the internal-temporal area, using proton magnetic resonance spectroscopy. Eleven patients with a mono-hippocampal epileptics focus on clinical and per-critical electroencephalographical criteria, were matched with 11 controls by age, sex and laterality. Proton spectroscopy of a volume of 8 cm3 was performed within the ipsilateral and the contralateral internal-temporal area and within the 2 hippocampus of controls. Volumetry of the ipsilateral and the contralateral hippocampus and of the 2 hippocampus of controls was performed using resonance magnetic imaging. All these measurements were performed during the interictal stage. The results were concordant to show a decrease of the ratio N-acetyl-aspartate/choline and N-acetyl-aspartate/creatine within the epilepticus focus, in relation with a hippocampal atrophy. This study finds similar results to those of other previous works. The decrease of N-acetyl-aspartate levels within the epilepticus focus could be related to a decrease of the neuronal cell density. This procedure is able to show a decrease of the levels of this metabolite within an internal temporal epilepticus focus and associated with a hippocampal atrophy.

Adolescent↗
PubMedDate not supplied

Left ventricular contractility after hypothermic preservation: predictive value of phosphorus 31-nuclear magnetic resonance spectroscopy.

Early graft failure accounts for a substantial portion of the mortality after heart transplantation. This factor underscores the need for the development of reliable methods for predicting graft performance and thus ensuring optimal clinical outcome. The aim of this study was to describe the link between myocardial metabolism evaluated throughout preservation with the use of phosphorus 31-nuclear magnetic resonance spectroscopy and ventricular contractility after reperfusion. Thirteen pig hearts were excised and preserved from 3 to 12 hours with clinical techniques. During preservation the hearts underwent phosphorus 31-nuclear magnetic resonance spectroscopy. After reperfusion, left ventricular contractility was evaluated with an isolated heart model undergoing isovolumetric contraction. Throughout storage, beta-adenosine triphosphate remained stable and intracellular pH and phosphocreatine decreased exponentially, whereas inorganic phosphate increased exponentially. Intracellular pH, phosphocreatine, inorganic phosphates measured at the onset of preservation, and intracellular pH and phosphocreatine measured at the end of preservation correlated significantly with the left ventricular contractility after reperfusion. We conclude that the metabolic state of myocardium at excision is especially important and that phosphorus 31-nuclear magnetic resonance evaluation of the heart during preservation appears to provide reliable indexes for predicting subsequent ventricular contractility after reperfusion.

Animals↗