Intravenous magnesium sulfate significantly increased the img 2 schoonheidssalon level in patients in group L from.35plus or minus0.06 mmol/L (mean plus or minus SD).54 plus or minus.09 mmol/L (p.01 and had an antiarrhythmic effect in 7 of the 8 patients (88). However, in group N patients, intravenous magnesium sulfate had an antiarrhythmic effect in only 1 of the 6 patients (17) (p.05 vs group L). These results suggest that intravenous magnesium sulfate may be effective in the acute management of cardiac arrhythmias in patients with a low serum iMg2 level. Ionic mechanisms of ischemia-related ventricular arrhythmias. Clinical Cardiology (usa 1996, 19/4 (325-331). The aim of this review is the utmost simplification of the cellular electrophysiologic background of ischemia-related arrhythmias. In the acute and subacute phase of myocardial infarction, arrhythmias can be caused by an abnormal impulse generation, abnormal automaticity or triggered activity caused by early or delayed afterdepolarizations (ead and dad or by abnormalities of impulse conduction (i.e., reentry).
Particularly in patients with one of these types of cardiac arrhythmias, however, it should be realized that preventing the patient from a magnesium deficit is the first, and the application of magnesium the second best strategy to keep the patient free from cardiac arrhythmias. Effect of intravenous magnesium sulfate on cardiac arrhythmias in critically ill patients with low serum ionized magnesium. Japanese circulation journal (Japan 1996, 60/11 (871-875). Magnesium affects cardiac function, although until the recent development of a new ion selective electrode no method existed for measuring the physiologically active form of magnesium, free ions (iMg2 in the blood. We investigated the antiarrhythmic effect of magnesium sulfate administered to critically ill patients with cardiac arrhythmias and reduced iMg2 as determined using the ion-selective electrode. Eight patients with a low iMg2 level (less than.40 mmol/L) were given intravenous magnesium sulfate (group L). Magnesium sulfate was also administered to patients with a normal iMg2 level (more than.40 mmol/L) but who did not respond to conventional antiarrhythmic drugs (group N).
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In 6 other cases of als and 5 neurologically normal controls it was found that aluminum concentrations in the precentral gyrus, internal capsule, crus cerebri and spinal cord were significantly higher in 2 als patients compared to the controls. Mean aluminum concentrations in 26 different central nervous system regions in the 2 patients were higher than controls and 4 of the als cases. Magnesium concentrations in 26 central nervous system regions were markedly reduced in the als cases. Calcium/magnesium ratios were significantly increased in als patients. The authors conclude that the high incidence of als in the western Pacific may be due to calcium/magnesium dismetabolism resulting in excess deposition of aluminum. Arrhythmia, magnesium in supraventricular and ventricular arrhythmias.
Zeitschrift fur Kardiologie (Germany 1996, 85/suppl. The use of magnesium as medical an antiarrhythmic agent in ventricular and supraventricular arrhythmias is a matter of an increasing but still controversial discussion during recent years. With regard to the well established importance of magnesium in experimental studies for preserving electrical stability and function of myocardial cells and tissue, the use of magnesium for treating one or the other arrhythmia seems to be a valid concept. In addition, magnesium application represents a physiologic approach, and by this, is simple, cost-effective and safe for the patient. However, when one reviews the available data from controlled studies on the antiarrhythmic effects of magnesium, there are only a few types of cardiac arrhythmias, such as torsade de pointes, digitalis-induced ventricular arrhythmias and ventricular arrhythmias occurring in the presence of heart failure or during.
Acute ethanol exposure (8-570 mM) induced potent contractile responses of rings in both basilar and middle cerebral arteries, from dogs, sheep, piglets and baboons, in a dose-dependent manner. The contractions were reproducible and not tachyphylactic. The middle cerebral arteries were found to be more sensitive to ethanol than the basilar arteries. No known pharmacological antagonist, tested, exerted any effects on ethanol-induced contractions. No differences in responsiveness to ethanol in canine arteries were found between male and female animals or between the presence and the absence of endothelial cells. Removal of extracellular Ca2 (Ca2)0) partially attenuated ethanol-induced contractions, while withdrawal of extracellular Mg2 (Mg2)0) potentiated such contractions.
In the complete absence of (Ca2)0, caffeine and ethanol induced similar, transient contractions followed by relaxation in K-depolarized cerebral vascular tissue. Ethanol-induced contractions were completely abolished by pretreatment of tissues with caffeine. Our results suggest that: (a) acute ethanol intoxication can induce direct contractions (independent of amine, prostanoid or opioid mediation) of diverse mammalian cerebral vascular tissues, including those from primates; (b) these contractile responses are heterogeneous along the cerebrovascular tree and independent of endothelial cells; (c). Amyotrophic Lateral Sclerosis, aluminum Deposition in Central Nervous System of Patients with Amyotrophic Lateral Sclerosis from the kii peninsula of Japan. Neurotoxicology, 1991; 615-620, low calcium/magnesium intake with excess amounts of aluminum and manganese are associated with the incidence of amyotrophic lateral sclerosis (ALS) in the western Pacific. Two japanese case reports of als showed markedly elevated concentrations of aluminum in the cns.
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Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and als cellular Ca2 concomitant with a progressive reduction in Mg content. Use of 31p-nmr spectroscopy coupled with optical-backscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose-dependent deficits in phosphocreatine (PCr the (PCr atp) ratio, intracellular pH (pH(i oxyhemoglobin, and branchiogene the mitochondrial level of oxidized cytochrome oxidase aa3, concomitant with a rise. Temporal studies performed in vivo, on the intact brain, indicate that (Mg2 i) is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg2 prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag-fura-2, on single-cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration-dependent depletion of (Mg2 i). These cellular deficits in (Mg2 i) seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to ca2 overload and ischemia. A role for ethanol-induced alterations in (Mg2 i) should also be considered in the well-known behavioral actions of alcohol. Ethanol-induced contraction of cerebral arteries in diverse mammals and its mechanism of action. (Netherlands 41993, 248/3 (229-236).
Alcohol-related, role of magnesium and reconstructie calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31p-nmr, spectroscopy and a unique magnesium ion-selective electrode. (usa 1994, 18/5 (1057-1068). It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg alcohol is now known to be the most notorious cause of Mg-wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free mg2 (Mg2 i which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators.
Thiosulphate pure, parameters, specifications, appearance, white Uniform Crystals (10 mesh) pH of 10 Aqueous Solution.5 to 8, assay 99 minimum Sulphites sulphates.2 max heavy metals Less than 5 ppm Iron Less than 10 ppm Sodium Thio sulphate Photographic. We can give the technical grade small crystals and large crystals too. Sodium Thiosulfate Anhydrous of similar specifications is offered Sodium Thiosulphate Anhydrous Specifications Formula (Na2) S2O3 Molecular weight 158 Assay as (Na2)S2O3 98 min. 10 solution in water Clear Description White powder free from foreign particles. PH of 10 solution.5.5 Sulphites sulphates.5 maximum Iron Less than 10 ppm heavy metals Less than 10 ppm Standard Packing. Hdpe bag with extra liner inside or in Jumbo bags or as required by the buyer.
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Muby Chemicals of Mubychem Group, established in 1976, is the original manufacturers of Specialty Chemicals, Pharmaceutical Excipient, Fragrance flavor chemicals, Shale gas Fracturing Chemicals in India. Mubychem Group has several manufacturing facilities spread across Western India and world wide contacts and toll manufacturers. We are exporting globally to countries like usa, canada, europe, uae, south Africa, tanzania, kenya, egypt, nigeria, cameroon, Uganda, turkey, mexico, brazil, Chile, argentina, dubai, korea, vietnam, Thailand, malaysia, indonesia, australia, china, germany, france, italy, portugal etc. The products are offered as per required specifications and in correct shape and size in mm or meshs or microns as specified by the buyer. The participating units have one or more accreditations like fda - gmp approval; iso-9001:2008 Certified; "reach" Pre-registered; iso-14001, iso-22000:2005, fssc 22000; iso ohsas 18001; Kosher Certified; Halal Certified; haccp, fssai. We offer Commercial Pure ip bp usp fcc food Grade acs ar analytical reagent Grades of Chemicals. Bookmark this Web Site, email This Page Info to a colleague or yourself. Search our website here, sodium thioulphate pentahydrate cas number, einecs ec number, hs code 283230 formula na2S2O3.5H2o, doen molecular weight 248.17. Sodium thioulphate anhydrous cas number, einecs ec number, hs code 283230 formula na2S2O3, molecular weight 158.11.