PubMed Health⌕ Search

Biomedical subjects

F Boucher

Publications and source records attributed to F Boucher.

At least 19 recordsLinked to original sources
PubMed2006

First-principles calculations within periodic boundary conditions of the NMR shielding tensor for a transition metal nucleus in a solid state system: The example of 51V in AlVO4.

We present the first density functional theory based calculations of NMR shielding parameters for a transition metal nucleus using periodic boundary conditions. These calculations employ the gauge-including projected augmented-wave pseudopotential approach. The quality of this method is discussed by comparing experimental and calculated chemical shift tensor eigenvalues for the quadrupolar 51V nucleus in the diamagnetic solid-state compound AlVO4. Furthermore, the combination of shielding tensor with fast and accurate projector augmented-wave electric field gradient tensor calculations allows us to determine the relative orientation of these two tensors.

Letter↗
PubMed2006

Antioxidant treatment prevents cardiac protein oxidation after ischemia-reperfusion and improves myocardial function and coronary perfusion in senescent hearts.

Cardiovascular ageing is associated with an increase in cardiac susceptibility to ischaemia and reperfusion and production of reactive oxygen species has been suspected to be responsible for this age-associated particular vulnerability. To determine whether administration of antioxidant treatment could afford some protection against ischaemia and reperfusion during aging, isolated perfused hearts from adult and senescent rats were submitted to normoxia (180 min), prolonged low-flow ischaemia (15% of initial coronary flow;180 min) or low-flow ischaemia/reperfusion (45 min/30 min), without or with antioxidant enzymes (superoxide dismutase+catalase; 50IU/ml). Contractile function and coronary perfusion were measured and protein oxidation was quantitated in left ventricle after normoxia, ischaemia and ischaemia/reperfusion. Protein oxidation was higher in senescent than in adult hearts after ischaemia-reperfusion, in contrast to prolonged ischaemia. During prolonged ischaemia, antioxidant treatment prevented coronary vasoconstriction at both ages and delayed contractile dysfunction in senescent hearts but did not limit protein oxidation. During reperfusion, antioxidant treatment prevented coronary vasoconstriction and protein oxidation at both ages and considerably improved recovery of contractile function in senescent hearts. In conclusion, antioxidant treatment fully protects the senescent heart against ischaemia/reperfusion but not against prolonged ischaemia injury, indicating that oxidative stress plays a central role in the age-associated vulnerability to ischaemia-reperfusion.

Aging↗
PubMed2004

New insights into the pathological role of TNF-alpha in early cardiac dysfunction and subsequent heart failure after infarction in rats.

A marked increase in plasma TNF-alpha has been described in patients with chronic heart failure (CHF). Nevertheless, little is known about the direct role of this cytokine early after myocardial infarction (MI) and its possible effects on the subsequent development of CHF. Wistar rats were subjected to permanent in vivo coronary artery ligation. At 5, 7, and 9 days after MI, cardiac function, passive compliance of the left ventricle (LV), and cardiac geometry were evaluated. The same model was used to perform pharmacological studies 7 days and 10 wk after MI in rats treated with monomeric recombinant human soluble TNF-alpha receptor type II (sTNF-RII, 40 microg/kg iv) or a placebo on day 3. Maximal alterations of cardiac function and geometry occurred 7 days after MI, which correlated chronologically with a peak of cardiac and serum TNF-alpha, as shown by immunohistochemistry and ELISA, respectively. sTNF-RII improved LV end-diastolic pressure under basal conditions and after volume overload 7 days and 10 wk after MI. Moreover, a significant leftward shift of the pressure-volume curve in the sTNF-RII-treated group 7 days after MI indicated a preservation of LV volume. Infarct expansion index was also significantly improved by sTNF-RII 7 days after MI (P < 0.01). Nevertheless, 10 wk after MI, geometric indexes and passive pressure-volume curves were not significantly improved by the treatment. In conclusion, TNF-alpha plays a major role in cardiac alterations 7 days after MI in rats and contributes to hemodynamic derangement, but not to cardiac remodeling, in subsequent CHF.

Animals↗
PubMed2003

Resveratrol and non-ethanolic components of wine in experimental cardiology.

The mechanisms through which the consumption of alcoholic beverages, in particular wine, protects against cardiac and vascular diseases remain largely unexplored. New methods are needed to investigate that crucial medical and scientific question. Several groups are now beginning to use animal models of myocardial ischemia and reperfusion to explore whether certain nutrients, including ethanol and non-ethanolic components of wine, may have a specific protective effect on the myocardium, independently from the classical risk factors involved in vascular atherosclerosis and thrombosis. Concepts used in experimental cardiology, such as preconditioning and stunning, are now entering the field of nutrition, and this will undoubtedly lead to considerable improvements in the prevention and treatment of cardiovascular diseases.

Animals↗
PubMed2003

Insulin resistance modifies plasma fatty acid distribution and decreases cardiac tolerance to in vivo ischaemia/reperfusion in rats.

1. The early stage of insulin resistance, also termed the 'prediabetic state', is characterized by the development of hyperinsulinaemia, which maintains normoglycaemia under fasting conditions. The metabolic disorders induced in myocardial cells during this stage of the disease may constitute a basis for an alteration of the tolerance of the heart to ischaemia and reperfusion. 2. To test this hypothesis, male Wistar rats were fed a 66% fructose diet for 4 weeks, inducing a prediabetic state. Rats were then subjected to in vivo left coronary artery ligation followed by reperfusion. Blood samples were collected for plasma lipid profile determination. 3. The prediabetic state significantly increased the severity of ischaemia-induced arrhythmias (arrhythmia score 1.4 +/- 0.2 vs 2.0 +/- 0.0 in control and fructose-fed rats, respectively; P < 0.05) and the size of infarction (infarct size 41.2 +/- 3.0 vs 56.0 +/- 2.0% in control and fructose-fed rats, respectively; P < 0.01). This alteration of the tolerance to in vivo ischaemia/reperfusion may be the consequence of an increase in mono-unsaturated fatty acids and a decrease in omega3 polyunsaturated fatty acids in fructose-fed-rats. 4. In conclusion, because it is known that the prediabetic state increases the incidence of cardiovascular diseases by promoting coronaropathy, our study suggests that this metabolic disorder may also affect the prognosis of heart disease by decreasing the tolerance of cardiomyocytes to ischaemic insults.

Animals↗
PubMed2001

Coronary and aortic vasoreactivity protection with endothelin receptor antagonist, bosentan, after ischemia and hypoxia in aged rats.

This study investigated the effects of bosentan, a dual endothelin ET(A) and ET(B) receptor antagonist, during hypoxia-reoxygenation of senescent aorta and during ischemia-reperfusion of senescent heart. Isolated aortic rings and isolated hearts from adult and senescent rats were submitted, respectively, to hypoxia/reoxygenation (20/30 min) and to low-flow ischemia/reperfusion (45/30 min), without or with bosentan (10(-5) M). In the aorta, bosentan treatment prevented the impairment of relaxation in response to acetylcholine after hypoxia-reoxygenation at both ages. In the heart, coronary flow recovery during reperfusion, which is lower in senescents than in adults (48% vs. 76% of baseline value, respectively; P<0.05) was fully prevented by bosentan. Prevention of endothelial dysfunction during reoxygenation of hypoxic aorta and of coronary vasoconstriction during reperfusion of ischemic heart with a dual endothelin ET(A) and ET(B) receptor antagonist suggests a role of endothelin in the vulnerability of aorta to hypoxia-reoxygenation, and of coronary arteries to ischemia-reperfusion, especially during aging.

Acetylcholine↗
PubMed2001

Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus.

The bHLH-PAS transcription factor SIM1 is required for the development of the paraventricular nucleus (PVN) of the hypothalamus. Mice homozygous for a null allele of Sim1 (Sim1(-/-)) lack a PVN and die perinatally. In contrast, we show here that Sim1 heterozygous mice are viable but develop early-onset obesity, with increased linear growth, hyperinsulinemia and hyperleptinemia. Sim1(+/-) mice are hyperphagic but their energy expenditure is not decreased, distinguishing them from other mouse models of early-onset obesity such as deficiencies in leptin and melanocortin receptor 4. Quantitative histological comparison with normal littermates showed that the PVN of Sim1(+/-) mice contains on average 24% fewer cells without a selective loss of any identifiable major cell type. Since acquired lesions in the PVN also induce increased appetite without a decrease in energy expenditure, we propose that abnormalities of PVN development cause the obesity of Sim1(+/-) mice. Severe obesity was described recently in a patient with a balanced translocation disrupting SIM1. Pathways controlling the development of the PVN thus have the potential to cause obesity in both mice and humans.

Adipose Tissue↗
PubMed2001

Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure.

BACKGROUND: Chronic heart failure (CHF) seems to be associated with increased oxidative stress. However, the hypothesis that antioxidant nutrients may contribute to the clinical severity of the disease has never been investigated. AIMS: To examine whether antioxidant nutrients influence the exercise capacity and left ventricular function in patients with CHF. METHODS: Dietary intake and blood levels of major antioxidant nutrients were evaluated in 21 consecutive CHF patients and in healthy age- and sex-matched controls. Two indexes of the severity of CHF, peak exercise oxygen consumption (peak VO2) and left ventricular ejection fraction (LVEF), were measured and their relations with antioxidants were analysed. RESULTS: Whereas plasma alpha-tocopherol and retinol were in the normal range, vitamin C (P=0.005) and beta-carotene (P=0.01) were lower in CHF. However, there was no significant association between vitamins and either peak VO2 or LVEF. Dietary intake (P<0.05) and blood levels of selenium (P<0.0005) were lower in CHF. Peak VO2 (but not LVEF) was strongly correlated with blood selenium: r=0.76 by univariate analysis (polynomial regression) and r=0.87 (P<0.0005) after adjustment for age, sex and LVEF. CONCLUSIONS: Antioxidant defences are altered in patients with CHF. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction. Further studies are warranted to confirm the data in a large sample size and to investigate the mechanisms by which selenium and other antioxidant nutrients are involved in CHF.

Adult↗
PubMed2001

Effect of wine ethanol on serum iron and ferritin levels in patients with coronary heart disease.

BACKGROUND AND AIM: The association between high body iron stores and coronary heart disease (CHD) is a subject of intense debate whereas wine consumption is known to be associated with a low CHD rate. It has been suggested that the inhibition of iron absorption is one of the possible mechanisms of the CHD-protective effects of drinking. METHODS AND RESULTS: We analysed the interrelationships of wine ethanol intake and fasting serum ferritin, iron and gamma glutamyl transferase (GGT) in patients enrolled in the Lyon Diet Heart Study, a secondary prevention trial designed to test whether a Mediterranean-type diet may protect against CHD. The intake of wine ethanol was evaluated in the 24 hours preceding blood sampling, and expressed as a percentage of the total daily energy intake. Data were obtained from 437 consecutive patients. There was a positive relationship (Spearman statistics) between wine ethanol and the serum levels of iron (r = 0.21, p < 0.0001), ferritin (r = 0.23, p < 0.0001) and GGT (r = 0.31, p < 0.0001). Uni- and multilinear regression analyses after excluding non-drinkers and log transforming the variables yielded similar results. CONCLUSIONS: The available data showing positive relationships between wine ethanol intake and serum concentrations of both ferritin and iron in patients with CHD tend to disprove the hypothesis that wine ethanol consumption could decrease iron stores and thereby the risk of CHD. Further studies are required to investigate the mechanism(s) by which wine drinking reduces the risk of CHD.

Aged↗
PubMed2000

Effects of selenium deficiency on the response of cardiac tissue to ischemia and reperfusion.

Over a 10-week period, female Wistar rats received a diet containing a low level of selenium, cofactor of the antioxidant enzyme glutathione peroxidase (GPx) in order to examine the influence of deficiency of this trace element (i) on tissue antioxidant enzyme defence systems, and (ii) on the susceptibility of the myocardium to ischemia-reperfusion injury. At the end of the dietary treatment, hearts were perfused at constant flow (11 ml/min) before being subjected to 15 min of global normothermic ischemia, followed by 30 min of reperfusion. The effects of selenium deficiency were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDevP, heart rate HR, and the product HR x LVDevP), as well as ultrastructural tissue characteristics. Furthermore, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured at the end of the reperfusion period. Results suggest that: (a) the activity of GPx is decreased by selenium deficiency while SOD activity remains unchanged, (b) the recovery of cardiac function and myocardial ventricular ultrastructure during reperfusion are altered in the selenium-deficient group compared to controls. These results illustrate the crucial role that selenium, the co-factor of one of the major antioxidant enzymes of the myocardium, plays in determining the vulnerability of the heart to ischemia and reperfusion.

Animals↗
PubMed2000

Effects of fasting and exogenous glucose delivery on cardiac tolerance to low-flow ischemia in adult and senescent rats.

Metabolic disorders due to changes in cytosolic glucose utilisation are suspected to be involved in the increased sensitivity of the aged myocardium to ischemia. This study presents the first direct measurement of glucose utilisation in hearts from senescent rats during low-flow ischemia under different conditions of substrate delivery and glycogen stores. Isolated hearts from young adult (4-months-old) and senescent (24-months-old) rats were subjected to 30 min coronary flow restriction (residual flow rate=2% of control flows). Experiments were performed using glucose-free or glucose-enriched (11 mmol/L) perfusion media. The effects of increased glycogen stores were assessed after 24-h fasting in both age groups. Ischemic contracture was measured via a left-ventricular balloon. Ageing increased ischemic contracture under both conditions of substrate delivery in fed rat hearts. The increase in ischemic tolerance induced by fasting in senescent rat hearts was less than that seen in young rat hearts. Moreover, fasting decreased glucose utilisation in hearts from young rats, an effect which was not found in hearts from old rats. Furthermore, myocardial glycogen utilisation was increased in all groups of aged rats compared with that of young adults, particularly under fasting conditions. It is concluded that fasting is less detrimental to the aged myocardium during low-flow ischemia than to the young myocardium because it does not further reduce exogenous glucose utilisation, and it stimulates glycogen consumption. Moreover, a reduction in exogenous glucose utilisation, which is only partly compensated for by increased glycogenolytic flux could be, at least in part, responsible for the increased ischemic contracture in hearts from old fed rats. Finally, our glucose-free experiments suggest that residual oxidative phosphorylation during low-flow ischemia might be less relevant in hearts from senescent rats than in those from young adults.

Aging↗
PubMed2000

A unique distortion in K1/3Ba2/3AgTe2: X-ray diffraction determination and electronic band structure analysis of its incommensurately modulated structure.

The incommensurately modulated structure of a square Te-net, namely that of K1/3Ba2/3AgTe2, is determined from single-crystal X-ray diffraction data within a (3+1)D higher dimension formalism. The phase is shown to crystallize in the monoclinic symmetry, P2(1)(alpha 0 gamma) superspace group with the following lattice parameters: a = 4.6441(10) A, b = 4.6292(12) A, c = 23.765(9) A, and beta = 101.28(2) degrees with q = 0.3248(6)a* -0.071(8)c*, that is, in a symmetry different from that reported for the average structure (tetragonal) or that assumed from electron diffraction measurements (orthorhombic). After the introduction of a crenel function for the Te displacive description, the refinement converged to a residual factor R = 0.033 for 2583 observed reflections and 115 parameters (R = 0.024 and 0.101 for 1925 main reflections and 658 first-order satellites, respectively). The [Ag2-Te2] and the Ba/K layers are found to be only weakly modulated. The modulation of the square Te-net is, however, both substantial and unique. Namely, it results in two different units: a "V"-shaped Te3 trimer and a "W"-shaped Te5 pentamer. To examine both unit types, which are segregated in domains that aperiodically alternate within the Te layers, first principles electronic band structure calculations were carried out for three model commensurate structures using the tight-binding linear-muffin-tin-orbital method (LMTO). The calculations show that the distorted structures of V-pattern (model 2) and W-pattern (model 3) are more stable than the average structure (model 1) and that the V-pattern distortion provides a slightly larger stabilization than does the W-pattern distortion. The Fermi surface calculated for the average structure shows nesting vectors that are consistent with the occurrence of the V- and W-pattern distortions in the Te layers. However, these vectors do not predict the observed modulation vector of the incommensurately distorted structure, because the stabilization energy associated with the distortion is not mainly dominated by the energy lowering of the occupied band levels near the Fermi level.

Journal Article↗
PubMed2000

Aging exacerbates hydrogen peroxide-induced alteration of vascular reactivity in rats.

Reactive oxygen species (ROS) such as superoxide anion (O2-*) and hydrogen peroxide (H2O2) can be produced by vascular endothelium and smooth muscle cells under diverse physiological and pathophysiological situations. These species are known to exert various deleterious effects by which they might induce changes in vascular reactivity. The aim of the present study was to evaluate the evolution of vascular susceptibility to H2O2 during aging in rats. Catalase activity was assessed in aortas from young adult (4 months) and aged (24 months) Wistar rats. In parallel experiments, isolated rings from both age groups were exposed to increasing doses of H2O2 (0, 0.1, 1, 5, or 10 mM) for 20 min and the residual vascular response to phenylephrine (PE = 10(-6) M) and acetylcholine (ACh = 10(-6) M) was evaluated. Our results indicate that aging increases aortic catalase activity (4 months: 0.20 +/- 0.02 IU/mg prot versus 24 months: 0.46 +/- 0.06 IU/mg prot, p < 0.001) while it exacerbates vascular sensitivity to H2O2. These results suggest that the observed increased H2O2-induced alterations of vascular reactivity during aging in rats might be due to increased sensitivity of the vasculature to ROS rather than to a decrease in the defense systems against these species.

Acetylcholine↗
PubMed2000

Structures and phase transitions of the A7PSe6 (A = ag, Cu) argyrodite-type ionic conductors. III. alpha-Cu7PSe6

The crystal structure of the third polymorph of the Cu(7)PSe(6) argyrodite compound, alpha-Cu(7)PSe(6), heptacopper phosphorus hexaselenide, is determined by means of single-crystal diffraction from twinned crystals and X-ray powder diffraction, with the help of extensive NMR measurements. In the low-temperature form, i.e. below the last phase transition, alpha-Cu(7)PSe(6) crystallizes in orthorhombic symmetry, space group Pna2(1), with a = 14.3179 (4), b = 7.1112 (2), c = 10.1023 (3) A, V = 1028.590 (9) A(3) (deduced from powder data, T = 173 K) and Z = 4. Taking into account a twinning by reticular merohedry, the refinement of the alpha-Cu(7)PSe(6) structure leads to the residual factors R = 0.0466 and wR = 0.0486 for 127 parameters and 3714 observed, independent reflections (single-crystal data, T = 173 K). A full localization of the Cu(+)d(10) element is reached with one twofold-, one threefold- and five fourfold-coordinated Cu atoms. The observation of two phase transitions for Cu(7)PSe(6), to be compared with only one for Ag(7)PSe(6), is attributed to the d(10) element stability in a low coordination environment, copper being less prone to lower coordination sites than silver, especially at low temperature.

Journal Article↗
PubMed2000

Structures and phase transitions of the A7PSe6 (A = Ag, Cu) argyrodite-type ionic conductors. II. Beta- and gamma-Cu7PSe6

The crystal structures of two of the three polymorphic forms of the Cu7PSe6 argyrodite compound are determined by means of single-crystal X-ray diffraction. In the high-temperature form, at 353 K, i.e. 33 K above the first phase transition, gamma-Cu7PSe6 crystallizes in cubic symmetry, space group F43m. The full-matrix least-squares refinement of the structure leads to the residual factors R = 0.0201 and wR = 0.0245 for 31 parameters and 300 observed independent reflections. In the intermediate form, at room temperature, beta-Cu7PSe6 crystallizes again in cubic symmetry, but with space group P2(1)3. Taking into account a merohedric twinning, the refinement of the beta-Cu7PSe6 structure leads to the residual factors R = 0.0297 and wR = 0.0317 for 70 parameters and 874 observed, independent reflections. The combination of a Gram-Charlier development of the Debye-Waller factor and a split model for copper cations reveals the possible diffusion paths of the d10 species in the gamma-Cu7PSe6 ionic conducting phase. The partial ordering of the Cu+ d10 element at the phase transition is found in concordance with the highest probability density sites of the high-temperature phase diffusion paths. A comparison between the two Cu7PSe6 and Ag7PSe6 analogues is carried out, stressing the different mobility of Cu+ and Ag+ and their relative stability in low-coordination chalcogenide environments.

Journal Article↗
PubMed1999

Effect of antioxidant trace elements on the response of cardiac tissue to oxidative stress.

It is now well established that several trace elements, because of their involvement in the catalytic activity and spatial conformation of antioxidant enzymes, may contribute to the prevention of oxidative stress such as occurs upon reperfusion of ischemic tissue. The aim of this paper is (1) to review the role of these trace elements (Cu, Mn, Se, and Zn) in antioxidant cellular defenses in the course of post-ischemic reperfusion of cardiac tissue, (2) to provide experimental data suggesting that variations in trace element dietary intake may modulate the vulnerability of cardiac tissue to ischemia-reperfusion, and (3) to discuss in more detail the effect of Mn ions, which seem to play a special protective role against reperfusion injury. Some results obtained from experiments in animal models of myocardial reperfusion have shown that the dietary intake of such trace elements can modulate cardiac activity of antioxidant enzymes and, consequently, the degree of reperfusion damage. In addition, experimental data on the protective effects of an acute treatment with Mn are presented. Finally, experimental evidence on the protective role of salen-Mn complexes, which exhibit catalytic SOD- and CAT-like activities against reperfusion injury, are described. These complexes should be of considerable interest in clinical conditions.

Animals↗