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C Abadie

Publications and source records attributed to C Abadie.

15 recordsLinked to original sources
PubMed1998

Demonstration of the production of oxygen-centered free radicals during electrolysis using E.S.R. spin-trapping techniques: effects on cardiac function in the isolated rat heart.

The present study was designed to identify the free radicals generated during the electrolysis of the solution used to perfuse isolated rat heart Langendorff preparations. The high reactivity and very short half-life of oxygen free radicals make their detection and identification difficult. A diamagnetic organic molecule (spin trap) can be used to react with a specific radical to produce a more stable secondary radical or "spin adduct" detected by electron spin resonance (ESR). Isovolumic left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were measured by a fluid-filled latex balloon inserted into the left ventricle. The coronary flow was measured by effluent collection. Electrolysis was performed with constant currents of 0.5, 1, 1.5, 3, 5, 7.5, and 10 mA generated by a Grass stimulator and applied to the perfusion solution for 1 min. A group of experiments was done using a 1.5 mA current and a Krebs-Henseleit (K-H) solution containing free radical scavengers (superoxide dismutase (SOD): 100 IU/ml or mannitol: 50 mM). Heart function rapidly declined in hearts perfused with K-H buffer that had been electrolyzed for 1 min. The addition of mannitol (50 mM) to the perfusion solution had no effect on baseline cardiac function before electrolysis while SOD (100 IU/ml) increased the coronary flow. However, SOD was more effective than the mannitol in protecting the heart against decreased of cardiac function, 5 min after the end of electrolysis. Samples of the K-H medium subjected to electrolysis were collected in cuvettes containing a final concentration of 125 mM 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and analyzed by spectroscopy. The ESR spectrum consisted of a quartet signal (hyperfine couplings aN = aH = 14.9 G) originating from the hydroxyl adduct signal, DMPO-OH. The intensity of the DMPO-OH signal remained stable during the 60 s of electrolysis and the quantity of free radicals induced by electrolysis was directly proportional to the intensity of the current. The addition of mannitol and SOD to the perfusate scavenged the hydroxyl radicals present in the solution, suggesting that both hydroxyl and superoxide radicals were formed during electrolysis.

Animals↗
PubMed1998

Vitamin E analogues reduce the incidence of ventricular fibrillations and scavenge free radicals.

The aim of our study was to analyse the protective effects of different alpha-tocopherol analogues 1) against fibrillations induced by an ischemia-reperfusion sequence, and 2) to further investigate in vitro the radical scavenging properties of these analogues by two sensitive methods. Concerning 1: isolated rat hearts underwent 10 min of coronary ligation followed by reperfusion and the alpha-tocopherol analogues were infused 15 min before occlusion. Functional parameters including heart rate and fibrillations were recorded. Concerning 2: the beta-phycoerythrin assay was utilised to determine the oxygen radical absorbing capacity (ORAC) of these vitamin E analogues against peroxyl radicals. Electron paramagnetic resonance (EPR) was used to measure their scavenger abilities on hydroxyl radical and superoxide anion production. Concerning 1: ventricular fibrillation times were reduced for all analogues treated hearts at concentrations of 1 microM and 5 microM, with Trolox being the most efficacious. Concerning 2: in our experimental conditions of intense production of free radicals, scavenging IC50 values for hydroxyl radical were 1.15, 2.17 and 4.04 mM for Trolox, MDL 74270 and MDL 74366 respectively. Superoxide anion IC50 values were 1.0 and 6.75 mM for Trolox and MDL 74270. Our results show that water-soluble analogues of vitamin E are effective in the prevention of coronary ligation induced reperfusion arrhythmia, under our experimental conditions. Moreover, our data demonstrate that these vitamin E analogues are effective scavengers for a variety of radicals. Our studies support the view that compounds that can either inhibit the formation or scavenge free radicals can protect the heart against arrhythmia associated with ischemia-reperfusion.

Animals↗
PubMed1997

Interleukin-1 beta and tumor necrosis factor-alpha inhibit the release of [3H]-noradrenaline from isolated human atrial appendages.

In the present study, we have investigated the ability of human recombinant interleukin-1 beta (hIL-1 beta) and human recombinant tumor necrosis factor-alpha (hTNF-alpha) to modulate the stimulation-induced (S-I) outflow of [3H]-noradrenaline ([3H]-NA) from isolated superfused human atria. Pieces of human right atrial appendages were excised during routine cardiac surgery. Tissues were incubated with [3H]-NA (0.2 mumol/l) for 30 min at 37 degrees C, then inserted in a Brandel suprafusion system where the radioactivity was washed for 75 min with a Krebs-Henseleit solution at a rate of 0.4 ml/min. Thereafter, the effluent was collected for the remainder of the protocol during which two trains of electrical stimulation (50 mA intensity, 5 Hz frequency, 60 s duration, 2 ms pulses) were delivered at 10 min and 45 min (short protocol) or 85 min (long protocol). The effect of drugs on the S-I outflow of [3H]-NA was determined by adding drugs 20 min (short protocol) or 60 min (long protocol) before the second stimulation. Experiments were carried out in the continuous presence of desipramine (1 mumol/l) to prevent neuronal NA reuptake. The results showed that in human atrium, hIL-1 beta (3 ng/ml) and hTNF-alpha (0.5 ng/ml) significantly inhibited the S-I release of [3H]-NA. The inhibitory effect of hIL-1 beta was blocked by human recombinant IL-1 receptor antagonist (50 ng/ml), and by the cyclooxygenase inhibitor, diclofenac (1 mumol/l), suggesting that hIL-1 beta inhibited NA release through the formation of prostaglandins. The ability of hIL-1 beta and hTNF-alpha to inhibit NA release suggest that mediators of the immune system produced locally may modulate the activity of the sympathetic nervous system in human atrial appendages.

Adult↗
PubMed1997

Beneficial actions of preconditioning and stretch on postischemic contractile function of isolated working rat heart: effects of staurosporine.

Preconditioning is commonly induced by a brief ischemic insult; myocardial stretch can trigger this protection by an unknown mechanism. Myocardial stretch preconditions the in vivo canine heart; however, the existence of a stretch-induced protection in the rat heart remains unknown. The purpose of this study was to test this myocardial protection induced, in isolated working rat heart, by global ischemia and stretch initiated by a transient increase in the left ventricle (LV). Isolated rat hearts underwent 30 min of global ischemia followed by 30 min of reperfusion. Before this, hearts received a 15-min period of either no intervention (control; C), 5 min of global ischemia + 10 min of reperfusion (preconditioning; PC) or 5 min of stretch + 10 min with no intervention (stretch; S). Stretch was induced by a transient increase in LV preload from 5 to 20 cm H2O. LV work started under a afterload of 80 cm H2O. Control, PC, and S hearts received either no drug (untreated) or staurosporine (50 nM), a protein kinase C inhibitor, before the "preconditioning" period. Creatine kinase (CK) release, ventricular fibrillation during reperfusion, and postischemic recovery of contractile function (aortic flow) were the end points of the study. In the S group, the abrupt increase in preload resulted in a significant increase of aortic flow (42 +/- 2 to 47 +/- 2 ml/min; p < 0.05). During the 30-min reperfusion period, control hearts displayed a poor recovery of contractile functions (8 +/- 3 ml/min, 30 min after reflow, versus 40 +/- 2 ml/min at baseline; p < 0.05). Both untreated PC and S groups exhibited a significant reduction in CK release, incidence of ventricular fibrillation (55% of control hearts developed persistent VF vs. 6% in both the PC and S groups), and postischemic dysfunction during reperfusion (p < 0.05 vs. control). Staurosporine prevented these beneficial effects in PC and S groups. Our study suggests that myocardial protection can be induced by stretch in the isolated working rat heart, likely through activation of protein kinase C. In conclusion, our results show that ischemic preconditioning and stretch had comparable favorable effect on functional recovery after a sustained ischemic insult in the isolated rat heart.

Animals↗
PubMed1996

Modulation of noradrenaline release from isolated human atrial appendages.

Prejunctional modulation of noradrenaline release has been studied extensively in various experimental preparations. However, the presence and importance of prejunctional noradrenaline release modulation in human cardiac tissue is still unclear. In this study, we have used superfused human right atrial appendages excised from patients undergoing open heart surgery. The tissues were cut into six pieces and incubated with [3H]noradrenaline (4 microCi/ml. 0.2 microM) for 30 min at 37 degrees C. The tissues were then inserted into a suprafusion system and washed for 75 min with a Krebs-Henseleit solution at a rate of 0.4 ml/min. The experimental protocol consisted of a 60-min perfusion period during which a field stimulation (2 ms pulses, 60 s. 50 mA, 5 Hz) was delivered at 10 and 45 min. The effect of the drugs on the stimulation-induced outflow of radioactivity was determined by adding them 20 min before the second stimulation. Each experiment was carried out with or without desipramine (1 microM) to study the influence of the reuptake blockade. Fenoterol (1-1000 nM), a beta 2-adrenoceptor agonist, and angiotensin II (1-1000 nM) significantly increased noradrenaline release in a concentration-dependent manner. The administration of arecaidine propargyl ester (0.03-3 microM), a non-specific muscarinic receptor agonist, and propylnorapomorphine (0.1 nM-1 microM), a DA2-dopaminergic agonist, produced a concentration-dependent inhibition of the stimulation-induced outflow of radioactivity. The alpha 2-adrenoceptor agonist, oxymetazoline (1 microM) inhibited noradrenaline release at a stimulation frequency of 2 Hz, but not at 5 and 10 Hz. The alpha 2-adrenoceptor antagonist, idazoxan (1 microM), significantly increased the release of noradrenaline at 2 and 5 Hz but not at 10 Hz. The results obtained in the present study demonstrated the presence of the facilitatory beta 2-adrenoceptor and angiotensin II receptor as well as the presence of inhibitory alpha 2-adrenoceptor, muscarinic and DA2-dopamine receptors in the human atrial appendage.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1996

Interleukin-1 beta and tumor necrosis factor-alpha inhibit the release of [3H]-noradrenaline from mice isolated atria.

In the present study, we have investigated the ability of four cytokines, interleukin-1 beta, interleukin-2, interleukin-6 and tumor necrosis factor-alpha, to modulate the stimulation-induced outflow of radioactivity from isolated superfused mouse atria which where pre-incubated with [3H]-noradrenaline. The tissues were subjected twice to field stimulation (5 Hz frequency, 50 mA intensity, 2 ms pulses for 60 s) and the drugs were added prior to the second stimulation in order to assess their modulatory effects. The results show that mouse recombinant interleukin-1 beta and tumor necrosis factor-alpha inhibited the stimulation-induced release of radioactivity from the isolated mouse atria. The effect of interleukin-1 beta was blocked by a human recombinant interleukin-1 receptor antagonist. The inhibitory effect of interleukin-1 beta was also abolished by the cyclooxygenase inhibitor, diclofenac (1 mumol/l) suggesting that the action of interleukin-1 beta might be mediated through the formation of prostaglandins. The effect of interleukin-1 beta appears to be time-dependent, since a stronger inhibition of radio-activity release was observed when the incubation time was increased from 20 to 65 minutes before the second stimulation. Interleukin-2 and interleukin-6 were ineffective in modulating release under these experimental conditions. The ability of interleukin-1 beta and tumor necrosis factor-alpha to inhibit noradrenaline release suggests that mediators of the immune system produced locally may modulate the activity of the sympathetic nervous system.

Animals↗
PubMed1995

Effect of in vivo heart irradiation on the development of antioxidant defenses and cardiac functions in the rat.

During radiotherapy of thoracic tumors, the heart is often included in the primary treatment volume, and chronic impairment of myocardial function occurs. The cellular biomolecules are altered directly by radiation or damaged indirectly by free radical production. The purpose of this investigation was to evaluate the biochemical and functional responses of the rat heart to a single high dose of radiation. The effect of 20 Gy local X irradiation was determined in the heart of Wistar rats under general anesthesia. Mechanical performances were measured in vitro using an isolated perfused working heart model, and cardiac antioxidant defenses were also evaluated. Hearts were studied at 1 and 4 months after irradiation. This single dose of radiation induced a marked drop in the mechanical activity of the rat heart: aortic output was significantly reduced (18% less than control values) at 1 month postirradiation and remained depressed for the rest of the experimental period (21% less than control 4 months after treatment). This suggests the development of myocardial failure after irradiation. The decline of functional parameters was associated with changes in antioxidant defenses. The decrease in cardiac levels of vitamin E (-30%) was associated with an increase in the levels of Mn-SOD and glutathione peroxidase (+45.5% and +32%, respectively, at 4 months postirradiation). However, cardiac vitamin C and catalase levels remained constant. Since these antioxidant defenses were activated relatively long after irradiation, it is suggested that this was probably due to the production of free radical species associated with the development of inflammation.

Aging↗
PubMed1994

Benzoselenazolinone derivatives designed to be glutathione peroxidase mimetics feature inhibition of cyclooxygenase/5-lipoxygenase pathways and anti-inflammatory activity.

Two series of compounds, substituted benzoselenazolinones and their opened analogs, diselenides, were prepared. The diselenides were designed according to the available SAR about glutathione peroxidase mimics and were expected to have activity. An initial series of tests was performed in order to assess the glutathione peroxidase and antioxidant activity of the diselenides compared to their cyclized analogs. The diselenides were shown to be very potent (up to 3 times the activity of ebselen), whereas the benzoselenazolinones were inactive, thus confirming our hypothesis. A second series of tests was done to determine the anti-inflammatory potency of the two series. Both were found to be potent on cyclooxygenase and 5-lipoxygenase pathways (up to 95% inhibition at 10(-5) M). Some compounds were selective, and the variations in the activity allowed us to draft some structure-activity relationships. The most interesting compound of each series, 6-benzoylbenzoselenazolinone and bis[(2-amino-5-benzoyl)phenyl] diselenide, was tested in vivo on the rat foot edema induced with different phlogistic agents and was shown to have some anti-inflammatory properties.

Animals↗
PubMed1994

Effect of cyclodextrins and undigested starch on the loss of chenodeoxycholate in the faeces.

Starch that escapes digestion in the small intestine increases the elimination of chenodeoxycholate and its metabolites in the faeces of both mice and hamsters. In contrast, the elimination of cholate and its metabolites is not increased. In vitro, the affinity of starch for chenodeoxycholate is about 90-fold greater than for cholate. beta-Cyclodextrin, which approximates to one turn of the helical structures formed by the 1,4-linked glucose units of starch, shares these properties. It is proposed that these helical structures in starch act as binding sites for bile salts.

Animals↗
PubMed1993

An alpha-tocopherol analogue with antioxidant activity improves myocardial function during ischemia reperfusion in isolated working rat hearts.

Recently, it has been reported that alpha-tocopherol analogues reduce infarct size in vivo in the rat and improve contractility upon reperfusion following global ischemia in isolated rat hearts. In the present study, we have thus investigated the effects of the hydrophilic alpha-tocopherol analogue MDL 74366 on nonenzymatic lipid peroxidation using a tissue homogenate method and reperfusion-induced arrhythmias following a local ischemia in isolated working rat hearts. Lipoperoxide (LPO) production was inhibited in a concentration-dependent manner in spontaneous as well as in induced peroxidations. The concentration resulting in a 50% inhibition (IC50) was around 2 microM. MDL 74366 treatment had no significant effect on baseline heart rate and cardiac output values. However, MDL 74366 decreased the incidence of reperfusion arrhythmias (ventricular tachycardia, VT; ventricular fibrillation, VF). The coincidence observed between the protective effect of MDL 74366 against tissue LPO formation and the preventive effect of this alpha-tocopherol analogue in the heart during the ischemia-reperfusion sequence confirms that vitamin E has beneficial effects against induced oxidative damage.

Animals↗
PubMed1993

Absence of relationship between antiarrhythmic effects of antidepressant drugs and lipid peroxidation.

Tricyclic antidepressant drugs may affect the cardiovascular system, principally in patients with preexisting cardiac disease. The present study was undertaken to compare the effects of amitriptyline and mianserin with those of tianeptine, an atypical tricyclic antidepressant drug, in rat isolated working heart subjected to a local myocardial ischemia. Coronary, aortic and cardiac flows, and heart rate remained stable during the whole preischemic period in control hearts. Ligation of the left main coronary artery induced a 50% decrease in coronary, aortic and cardiac flow without any change in heart rate. Reperfusion was characterized by the occurrence of ventricular arrhythmias (ventricular tachycardia and ventricular fibrillation) and by a marked reduction in cardiodynamic parameters. Amitriptyline (1 and 10 mumol/l) and mianserin (1 and 10 mumol/l) exhibited an antiarrhythmic activity against reperfusion arrhythmias. Tianeptine (1 and 10 mumol/l) was not able to reduce the incidence of reperfusion arrhythmias. Although tianeptine did not change heart rate, mianserin and amitriptyline induced a bradycardia. Mianserin and amitriptyline improved the cardiac recovery of cardiac function during reperfusion. The cardiodynamic parameters (coronary, aortic and cardiac flows) were not altered by tianeptine during the preischemic period. Furthermore, these parameters were similar to those observed in the control group both during ischemia and reperfusion. The beneficial effects of amitriptyline and mianserin observed in the setting of myocardial reperfusion were not associated with a reduced lipoperoxidation investigated by using an in vitro model in the presence or absence of a free-radical-generating system. The results of the present study indicate that the pronounced antiarrhythmic activities of mianserin and amitriptyline cannot be explained by an antiperoxidative action of these drugs.

Amitriptyline↗
PubMed1991

[Early management of language disorders].

The audio-language consultations of the Centre d'Audiophonologie of Lyon, France, allow the diagnosis of language delay to be documented in very young children. Based on a five-year clinical study, the authors propose a method of regular follow-up for the child and the parents.

Age Factors↗
PubMed1989

[Not Available].

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Balneology↗