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M Bara

Publications and source records attributed to M Bara.

At least 37 records · Page 2Linked to original sources
PubMed1997

Implication of external Mg2+ ions in the depolarization of smooth muscle cell membrane of the human chorionic placental vessels: an hypothesis.

The membrane potential (MP) of the smooth muscle cells of human allantochorial placental vessels is the major factor which explains the excitation-contraction coupling. Indeed, the smooth muscle cells of these vessels may be considered as tonic because they only respond to excitatory stimuli with graded depolarization. On the contrary, the phasic smooth muscles generate action potentials and some generate electrical slow waves as well. The depolarization of smooth muscle cell membranes may be a consequence of various factors, particularly the secretion of endothelium-derived depolarizing factors (EDDF). The modifications of the ionic composition of external medium interfere with the membrane potential values. The increase of [Mg2+]o (Cl- or SO4[2-]) depolarizes the membrane. This effect in vitro seems inconsistent with the known vasodilator action of external Mg2+. To explain this result, an hypothetical scheme is proposed on the probable targets of local and systemic Mg2+ effects: a direct action of external Mg2+ ions on the membrane potential by secretion of depolarizing endothelial factors which depolarize the membrane; an indirect action on the membrane potential by regulation of K+ and Ca2+ channels; an action on the concentration of internal Mg2+; an interaction with internal Ca2+ concentration and regulation of the Na+/Ca2+ exchanger. A data review of Mg2+ ions effects on smooth muscles is realized to corroborate this scheme.

Animals↗
PubMed1997

Neurotic, neuromuscular and autonomic nervous form of magnesium imbalance.

The nervous form of magnesium imbalance represents the best documented experimental and clinical aspects of magnesium disorders. The nervous form of primary magnesium deficit (MD) in the adult appears as the best descriptive model for analysis of the symptomatology, aetiology, physiopathology, diagnosis and therapy of the most frequent form of MD. Nervous hyperexcitability due to chronic MD in the adult results in a non-specific clinical pattern with associated central and peripheral neuromuscular symptoms, analogous to the symptomatology previously described in medical literature as latent tetany, hyperventilation syndrome, spasmophilia, chronic fatigue syndrome, neurocirculatory asthenia and idiopathic Barlow's disease. On encountering this non-specific pattern, the signs of neuromuscular hyperexcitability are of much greater importance. Trousseau's sign is less sensitive than Chvostek's sign, but their sensitivities are increased by hyperventilation (Von Bondsdorff's test). Examination of the precordial area will be conducted in order to search clinical stigmata of mitral valve prolapse (MVP) which is a frequent dyskinesia due to chronic MD (about a quarter to one-third of cases). The electromyogram (EMG) shows one (or several) trains of autorhythmic activities beating for more than 2 min of one of the three tetanic activities (uniplets, multiplets or 'complex tonicoclonic tracings') during one of the three facilitation procedures: tourniquet-induced ischaemia lasting 10 min. post-ischaemia lasting 10 min after the removal of the tourniquet and hyperventilation over 5 min. A repetitive EMG constitutes the principal mark of nervous hyperexcitability (NHE) due to MD. The echocardiogram (ECC) is the best tool for detecting MVP, the 2-dimensional ECC with pulsed Doppler being more accurate than time-motion ECC. The routine ionic investigations comprise five static tests: plasma and erythrocyte magnesium, plasma calcium and daily magnesiuria and calciuria. An evaluation of magnesium intake is desirable. Normal concentrations of magnesium in blood do not rule out the diagnosis of the nervous form of primary chronic MD. The histograms of MD group reveal Gaussian type magnesaemias with significantly lower means and the constituent elements can be individually hypo- (one-third of cases), normo- (about two-thirds of cases) and even, exceptionally, hyper-magnesaemic. The diagnosis of MD requires an oral magnesium load test. At physiological dose (5 mg of Mg/kg/day), oral magnesium is totally devoid of the pharmacological effects of parenteral magnesium. Corrections of symptomatology by this oral physiological magnesium load is the best proof that it was due to magnesium deficiency. In particular clinical forms, more sophisticated studies may be useful: standard and quantitative electroencephalograms, electropolygraphic studies of afternoon sleep, electronystagmography, optokinetic test, skin conductance reflex, psychometric inventories, standard or monitoring electrocardiogram, treadmill test, other static and dynamic investigations: e.g. ionized free Mg2+, lymphocyte Mg, brain Mg, cerebrospinal Mg, Mg balance, Mg parenteral load test, glucose load, and even radio-isotope study, the only one able to reveal intestinal magnesium hypersecretion. Nervous primary chronic MD progresses by phases of decompensation against a background of latency. Marginal magnesium deficiency, that is to say an insufficient magnesium intake which merely requires simple oral physiological supplementation, is fundamental in the aetiology of primary magnesium deficit. However a constitutional homeostatic lability of the nervous system or of magnesium metabolism such as belonging to the B35 type of HLA group must be involved. Part of the aetiology of this magnesium deficit is a magnesium depletion, where the disorder which induces magnesium deficit is related to a dysregulation of the control mechanisms of magnesium status which requires a more or less difficult

Administration, Oral↗
PubMed1997

Comparative experimental study of Mg lactate, vitamin B6 and their association on the permeability of a human membrane. 1. Effect on the total ionic transfer through isolated amniotic membrane.

The effects of Mg lactate, vitamin B6 and their association were studied on the ionic transfer through a membranous model: the human isolated amniotic membrane. The ionic transfer was evaluated by measuring of the total conductance in the maternal to fetal way (GtM) and in the fetal to maternal way (GtF) and of the ionic fluxes (F1 on the maternal side, F2 on the fetal side) and of the ratio F1/F2. Whatever the concentration, Mg lactate decreased GtM, F1, F2, F1/F2 but had a concentration-dependent effect on GtF. Vitamin B6 had no significant effect on GtF, F1, F2, F1/F2, but decreased GtM whatever its concentration. The association Mg lactate + vitamin B6 presented a biphasic action on GtM, GtF, F1, F2 and F1/F2: decrease at low ratio and increase from ratio equal to 8. This association induced interesting effect in the case of therapeutic use in comparison with the effects of separated compounds.

Amnion↗
PubMed1997

Are age-related neurodegenerative diseases linked with various types of magnesium depletion?

Age-related human neurodegenerative diseases are a major social and medical problem. It is therefore logical to take into consideration every theory with an overall approach to neurodegenerative diseases. This environmental proposal relies mainly on data concerning the Western Pacific amyotrophic lateral sclerosis-Parkinsonism-dementia complex (WP ALS-PD) considered as 'a prototypal human neurodegenerative disease' and on extrapolation from it to the bulk of neurodegenerative diseases (NDD). NDD would be due to an accelerated ageing process in certain populations of neurons due to the noxious synergy of (1) increased environmental slow deleterious factors (such as slow toxins) and of (2) decreased environmental protective factors (Mg deficient intake particularly). First, it was observed that three apparently dissimilar conditions occurred at extraordinary high rates in the Guam area: motoneuron disease (ALS), Parkinson's disease (P) and Alzheimer's-like dementia (D). Next, several other foci of endemic ALS-PD were found in Asia and Oceania in three Western Pacific population groups. These included the Chamorro people in Mariana Islands (Guam and Rota), the Auyu and Jakai people of West New Guinea and the Japanese residents of the Kii peninsula (Honshu island). The post-Second World War decline of the occurrence of WP ALS-PD in all three high incidence disease foci coupled with the absence of demonstrable heritable or transmissible factors had led to focus the search for the cause of this degenerative disease on nontransmissible environmental factors that are disappearing as the susceptible population groups acculturate to modern way. Epidemiologic study has shown that preference for traditional Chamorro food is the only one of 23 tested variables significantly associated with an increased risk for PD. An early suggestion incriminated the toxic seed of the false sago palm (Cycas circinalis L) which was used in traditional food and medicine. Laboratory investigation of cycad seed revealed the presence of various toxins and particularly of an 'unusual' non protein aminoacid: L-BMAA (beta-N-methylamino-L-alanine), an excitotoxic aminoacid. This slow toxin presents some structural similarity to another 'unusual' excitotoxic aminoacid: L-BOAA (beta-N-oxalyl-amino-L-alanine), an exogenous neurotoxin present in the grass pea (Lathyrus sativus) whose excessive consumption may cause lathyrism. The excitotoxicity of both L-BMAA and L-BOAA mainly concerns non-NMDA receptors. The neurotoxicity of these aminoacids varies with experimental models failing to induce an experimental model akin to WP ALS-PD or displaying many of the motor-system and behavioral changes of WP ALS-PD. It may be due to the presence of physiological levels of bicarbonate or of various toxic cofactors: bio-organic such as cycasin or inorganic such as pollutant metals e.g. aluminum or manganese, together with the lack of protective factors (e.g. calcium and magnesium deficiencies). Combined Al intoxication with Ca-Mg deficiencies is a reasonable model to investigate the pathogenesis of neurodegenerative diseases and eventually to screen their treatments. It may also be considered as a model of magnesium deficit, but it does not concern simple magnesium deficiency reversible with mere oral physiological magnesium supplementation. Magnesium deficiency cannot result in neurodegenerative disease. Combined Al intoxication with Ca-Mg deficiencies is not reversible through physiological oral magnesium supplementation. It therefore constitutes a type of experimental magnesium depletion model, instrumental in the investigation of the pathogenesis of magnesium depletion and in the screening of its still unknown possible treatments. (ABSTRACT TRUNCATED)

Aging↗
PubMed1996

Nuclear microanalysis of the effect of magnesium and taurine on the ionic distribution in the human amniotic membrane.

The effect of the addition of MgCl(2) and of taurine on the concentration and distribution of ions, present in physiological fluid, in epithelial (EL) and compact (CL) layers of the human amniotic membrane has been investigated using the Bordeaux nuclear microprobe. Particle induced X-ray emission and Rutherford backscattering spectrometry techniques had been used to provide quantitative measurements. In physiological medium (Hanks' solution), the monovalent ions (Na+, K+, Cl-) concentrations were identical in both layers. This data indicates that the compact layer acts as a buffer which fix minerals. Mg(2)+, Ca(2)+ and phosphorus levels were higher in EL than in CL. The addition of MgCl(2) in Hanks' solution induced a decrease of the monovalent ions concentration in both layers except Na+ level in EL which remained constant, an increase of the Mg(2)+ level in both layers while the Ca(2)+ and phosphorus remained constant. Addition of taurine in the Hanks' solution implicated several observations: taurine had no effect on the Na+, Mg(2)+, Ca(2)+ and phosphorus levels in EL and CL, but decreased the K+ and Cl- concentrations in both layers. The quantitative results may be related to electrophysiological observations on ionic exchanges through channels and paracellular pathways. The nuclear microanalysis processing may be of great interest to explain pregnancies complicated by poly or oligohydramnios.

Amnion↗
PubMed1995

Comparative studies of Ca N-acetylhomotaurinate and Ca N-acetyltaurinate. I. Effects on the ionic transfer through the isolated human amnion.

The effects of two taurine and homotaurine derivatives (Ca N-acetyltaurinate: ATACa and Ca N-acetylhomotaurinate: AOTACa) were studied on the ionic transfer through a membranous model: the human isolated amniotic membrane. The ionic transfer was evaluated by measurements of the various components (cellular and paracellular) of the total conductance across the membrane. AOTACa influenced all the components of the total ionic conductance without flux ratio modifications and the general action scheme was a biphasic effect: decrease conductance with low concentrations and increase conductance with high concentrations. This effect might be important in the case of lower or higher supplementation. ATACa only interfered with some conductance components and this action was predominantly monophasic (decreased or increased conductance). This study indicates differential actions between two closely related molecules on a membranous model.

Acamprosate↗
PubMed1995

Membrane potential of smooth muscle cells of human placental chorionic vessels. Comparative effects of MgCl2 and MgSO4.

Magnesium has been shown to produce various effects on vascular smooth muscle, in that its absence elicits an increase in muscle tone and increases sensitivity to a number of stimulatory agonists. In the present study, the influence of MgCl2 and MgSO4 was investigated in human placental chorionic muscle cells (from arteries and veins with or without endothelium), especially on the membrane potential, Um. Classically, Um was obtained from microelectrodes inserted into smooth muscle cells through the endothelium or directly. In arteries with endothelium, the smooth muscle cells were depolarized by MgSO4 (threshold: 6 mM) and MgCl2 (threshold: 8 mM). In endothelium-free arteries, the smooth muscle cells were also depolarized by MgSO4 (threshold: 8 mM) and MgCl2 (threshold: 6 mM). Identical results were obtained with veins, but thresholds were different. The different thresholds may indicate that MgCl2 influences the cell membrane potential directly, while MgSO4 interferes first with the endothelial cells, which may act as an intermediary between the Mg2+ ions and the membrane of the smooth muscle cells.

Dose-Response Relationship, Drug↗
PubMed1995

Nuclear microanalysis of the monovalent ion distribution in the human amnion. I. Effect of magnesium.

The effect of the addition of MgCl2 on the Na+, K+, and Cl- concentration and distribution in epithelial and compact layers of the human amniotic membrane was investigated using the Bordeaux nuclear microprobe. Particle-induced X-ray emission and Rutherford backscattering spectrometry techniques were used to provide quantitative measurements. In physiological medium (Hanks' solution), the monovalent ion concentrations were identical in both layers. The addition of Mg2+ ions in Hanks' solution induced a decrease of, K+, and Cl- concentration in both layers and, Na+ concentration in the compact layer. The results obtained from nuclear microanalysis might be explained from electrophysiological data which indicate that the addition of Mg2+ ions results in an increase in the cellular, paracellular and exchanger ion pathways.

Amnion↗
PubMed1995

Influence of magnesium salts on the membrane potential of human endothelial placental vessel cells.

Magnesium salts have been shown to depolarize the membrane of the smooth muscle cells of human placental arteries and veins with and without endothelial cells. In the present study, the influence of MgCl2 and MgSO4 was investigated on the membrane potential, Um, of the endothelial cells of the same vessels. Um was classically recorded with microelectrodes. The endothelial cell membrane of arteries was depolarized by MgCl2 (depolarization threshold, d th: 4 mM) and by MgSO4 (d th: 8 mM). A depolarization was also observed with the endothelial cell membrane of veins. The depolarization threshold with MgCl2 and 4MgSO4 was respectively 6 mM and 8 mM. The different thresholds indicate that the influence of MgCl2 on the endothelial cell membrane potential is higher and more direct than that of MgSO4, and confirm previous hypothesis on the effects of magnesium salts on the vascular smooth membrane cells.

Electric Stimulation↗
PubMed1994

Magnesium and therapeutics.

Two different types of therapy with magnesium are used: physiological oral magnesium supplementation which is totally atoxic since it palliates magnesium deficiencies by simply normalizing the magnesium intake and pharmacological magnesium therapy which may induce toxicity since it creates iatrogenic magnesium overload. Primary and secondary magnesium deficiencies constitute the sole indication of physiological oral magnesium therapy. It is therefore necessary to be well acquainted with the clinical and paraclinical pattern of magnesium deficit and to discriminate between magnesium deficiency due to an insufficient magnesium intake which only requires oral physiological supplementation and magnesium depletion related to a dysregulation of the control mechanisms of magnesium status which requires more or less specific regulation of its causal dysregulation. Physiological oral magnesium load constitutes the best tool for diagnosis of magnesium deficiency and the first step of its treatment. Physiological oral magnesium supplementation (5 mg/kg/day) is easy and can be carried out in the diet or with magnesium salts, with practically only one contra-indication: overt renal failure. Specific and aspecific treatments of magnesium depletion are tricky using for example magnesium sparing diuretics, pharmacological doses of vitamin B6, physiological doses of vitamin D and of selenium. In order to use the pharmacological properties of induced therapeutic hypermagnesaemia, high oral doses of magnesium (> 10 mg/kg/day) are advisable for chronic indications and the parenteral route is suitable for acute indications. There are 3 types of indications: specific (for the treatment of some forms of magnesium deficit i.e. acute), pharmacological (i.e. without alterations of magnesium status) and mixed--pharmacological and aetiopathogenic--(for example complications of chronic alcoholism). Today pharmacological magnesium therapy mainly concerns the obstetrical, cardiological and anaesthesiological fields. The main indications are eclampsia, some dysrhythmias (torsades de pointe particularly) and myocardial ischaemias. But it is now difficult to situate the exact place of the pharmacological indications of magnesium. Magnesium infusions can only be envisaged in intensive care units with careful monitoring of pulse, arterial pressure, deep tendon reflexes, hourly diuresis, electrocardiogram and respiratory recordings. High oral magnesium doses besides their laxative action may bring latent complications which may reduce lifespan. There may remain some indications of the laxative and antacid properties of non soluble magnesium, particularly during intermittent haemodialysis. Lastly local use of the mucocutaneous and cytoprotective properties of magnesium is still valid, in cardioplegic solutions and for preservation of transplants particularly.

Administration, Oral↗
PubMed1994

Inhibitor effects on the ionic exchanges through the human amniotic epithelial cell membranes.

Direct measurements of cell podocyte/or microvillous membrane ionic exchanges were performed on the membranes of isolated human amniotic epithelial cells. The ionic exchanges were determined from the measures of cellular input conductances. The effects of various inhibitors: ouabain, amiloride, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), 4'4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), quinidine, barium, manganese were analyzed. This study shows that the ionic exchanges through the epithelial cells are regulated by the presence of Na+,K+,Cl- channels, Na+/H(+)-Cl-/HCO3- antiports, (Na-K)ATPase and Na+/Ca(2+)-Na+/Mg2+ exchangers on the 2 faces of the cells and of a Na(+)-K(+)-2Cl- cotransport on the membrane facing the amniotic cavity only.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Effect of magnesium supplement in a biological medium (milk) on multiple ionic exchangers in a human membrane.

The effects of magnesium supplement in a biological medium (milk) diluted in a survival medium (1/20 dilution in Hanks' solution) have been studied on the multiple ionic exchangers in a human membrane, the amniotic membrane, which is a leaky and asymmetrical membrane. In normal milk, the Ca/Mg molar ratio (MR) is equal to 6.0. In this study, this ratio has been modified to between 0.36 and 6.0, with particular attention to MR values of 0.36, 0.6, 1.0, and 2.0. The transamniotic conductance, Gt, is a function of the Ca/Mg MR: Gt decreases when the MR increases from 0.36 to 6.0, with an inflexion point to 0.7. In the human amnion, Gt is the sum of three paracellular components (Gp) and nine cellular components (Gc). The addition of normal milk (MR = 6) or magnesium-supplemented milk (MR = 0.36, 0.6, 1.0 or 2.0) induces variation in 2 Gp (GpNa and GpK) and three cellular conductances (Na+ and K+ channels and Na/Mg exchanger). Among the MR values studied, MR = 0.36 increased all five components. These data show the relationship between magnesium and milk components and the cellular targets of magnesium supplements and define the best Ca/Mg molar ratio in the biological medium.

Amnion↗
PubMed1994

Comparative effects of MgCl2 and MgSO4 on the ionic transfer components through the isolated human amniotic membrane.

The effects of MgCl2 and MgSO4 are different on the total transfer through the human amniotic membrane: MgCl2 at low concentration (1 mM) decreases the total conductance Gt and increases it at high concentration (4 mM) on the fetal side (FS) and on the maternal side (MS), while MgSO4 has no effect on the MS and increases Gt on the FS. Moreover, whatever the concentration, MgCl2 increases the flux ration F1/F2 while MgSO4 decreases it to reach a value near to 1. Gt is the sum of various components: three paracellular components (Gp) and nine cellular components (Gc constituted from channels, exchangers, antiporters and cotransporters). All components of Gt, on the two faces, are decreased by 1 mM MgCl2 and increased at 4 mM. MgCl2 also has an effect on all ionic exchangers across the membrane. In contrast, on the MS, MgSO4 (1 mM) decreases GpNa, increases GpK and the antiport Na/H component and has no effect on any of the other components, while at 4 mM, MgSO4 has no effect. On the FS, MgSO4 (1 mM) increases GpNa and GpK, but does not modify the other components. At 4 mM, the effect is the same, except for an increase of GpCl. These data show the importance of the anion-cation association in the ionic exchanges through a membrane: MgCl2 and MgSO4 have a different action--MgCl2 interacts with all the exchangers, while the effect of MgSO4 is limited to paracellular components without interaction with cellular components excepted the antiport Na/H.

Amnion↗
PubMed1993

Magnesium effect on the membrane potential of smooth muscle cells of human placental chorionic vessels.

The effects of magnesium ions were studied in human placental chorionic vessel smooth muscle cells (from arteries and veins), particularly on the membrane potential Um. Um was classically recorded with microelectrodes. Magnesium ions, in the range 1-10 mM, depolarize the membrane of the smooth muscle cells (the effect is more important in arteries than in veins). Magnesium ions influence the membrane potential directly and regulate the viability of the K+ channels.

Arteries↗
PubMed1993

Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly.

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.

Adrenocortical Hyperfunction↗