[Note on the action of sodium sulfate, magnesium sulfate and magnesium chloride on rinderpest virus adapted to cell culture].
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Magnesium sulfate, at dose levels of 250, 500 and 1000 mg/kg, was administered subcutaneously three times daily to Crj:CD(SD) female rats from day 15 through day 20 of gestation. The effects of the compound on dams and F1 animals were examined. In the dams, decreased food consumption was observed in the 500 and 1000 mg/kg groups. Hypolocomotion, pronation, bradypnea and decreased body weight gain were observed in the 1000 mg/kg group. But there were no effects on the delivery or lactation conditions and necropsy from administration of the test article. In the F1 animals, low body weight, delays in differentiation (eruption of lower incisor, opening of eyelid) and reversible change in ribs (wavy rib) were observed in the 1000 mg/kg group. But there were no effects from administration of the test article in viability, functional examinations, behavior tests or reproductive ability. Based on the above results, under the conditions of this study, it was concluded that the non-toxic dose levels for general toxicological effects on dams was 3 x 250 mg/kg/day, for reproductive ability of dams was 3 x 1000 mg/kg/day, and for development of F1 animals was 3 x 500 mg/kg/day.
Potential for increasing contamination of water supplies with such materials as dissolved inorganic solids suggests more precise water quanlity standards for poultry. Commercial strain S.C.W.L. hens were supplied water containing sodium sulfate (Na2SO4) or magnesium sulfate (MgSO4) (250, 1,000, 4,000, or 16,000 p.p.m.) on a total sulfate basis in Exp. 1 and on a total salt basis in Exp. 2. All data are expressed as percentages deviated from pre-treatment performance. Four thousand p.p.m. of total sulfate as Na2SO4 or MgSO4 significantly depressed feed consumption and hen-day production. Magnesium sulfate (4,000 p.p.m.) had a more depressing effect than Na2SO4 (4,000 p.p.m.) on hen-day production (-80.4 vs. -24.4%). At that level, Na2SO4 significantly increased water consumption and fecal moisture content, while MgSO4 significantly decreased water consumption. All hens on 1l,000 p.p.m. of either salt died during the experiment. No effect on egg quality was observed before the hens died. On a total salt basis (Exp. 2) 16,000 p.p.m. of either Na2SO4 or MgSO4 significantly depressed hen-day production, body weight, and feed comsumption, but increased water consumption. Hens receiving 16,000 p.p.m. Na2SO4 increased water consumption more than those receiving 16,000 p.p.m. MgSO4(146.7 and 24.6%). No significant differences between treatments were observed for mortality (Exp. 2). Mortality data suggest that lethal levels of Na2SO4 and MgSO4 are between 16,000 and 20,032 or 23,680 p.p.m. total salt, respectively.
Markovitz, Alvin (University of Chicago, Chicago, Ill.) and Susan Sylvan. Effect of sodium sulfate and magnesium sulfate on heteropolysaccharide synthesis in gram-negative soil bacteria. J. Bacteriol. 83:483-489. 1962.-The effect of Na(2)SO(4) and MgSO(4) on heteropolysaccharide biosynthesis has been investigated in gram-negative bacteria isolated from soil. These bacteria may be divided into three arbitrary groups on the basis of the effect of Na(2)SO(4) and MgSO(4) on heteropolysaccharide synthesis: group 1, synthesis of polysaccharides containing uronic acid is inhibited by increasing the concentration of sulfate ion; group 2, synthesis of polysaccharides containing uronic acid is stimulated by sulfate ions; group 3, synthesis of polysaccharide not containing uronic acid is stimulated minimally by Na(2)SO(4).
Magnesium deficiency, prostacyclin deficiency and reduced prostacyclin sensibility of the thrombocytes may possibly play an important pathophysiological role in gestosis/pre-eclampsia. For this reason, we studied the influence of magnesium sulphate (in vitro 2-16 mVal/l) on thromboelastogram, spontaneous and ADP-induced thrombocyte aggregation, prostacyclin sensitivity of the thrombocytes and prostacyclin liberation from umbilical cord vessel preparations. The thromboelastogram showed an inhibitory influence of magnesium sulphate on all measurement parameters. Spontaneous and ADP-induced thrombocyte aggregation were inhibited to a statistically significant extent. The prostacyclin sensibility of the thrombocytes was increased by magnesium-sulphate. Magnesium sulphate enhanced prostacyclin liberation from the vascular wall significantly by 20-36%. It is possible that in gestosis magnesium sulphate may exercise a favourable influence on the disturbed balance between prostacyclin production and prostacyclin sensibility of the thrombocytes by exercising an influence on coagulation, thrombocyte function and prostacyclin liberation, and that it can thus contribute towards stabilising coagulation disturbances.
Preterm labor becomes more difficult to inhibit as the degree of cervical dilation increases. Indeed, some physicians do not even attempt tocolysis with advanced cervical dilation. We compared single- versus double-agent tocolytic therapy when the cervix was dilated 3 cm or greater. We conducted a retrospective study of 44 patients with preterm labor of unknown etiology and with cervical dilation of greater than 3 cm. At the admitting physician's discretion, patients were treated with either magnesium sulfate or with magnesium sulfate and indomethacin in combination. Longer duration of successful tocolysis was noted in the group that received both magnesium sulfate and indomethacin (368.3 hours versus 70.9 hours). No maternal complications occurred in either group. These pilot data suggest that tocolysis with magnesium sulfate and indomethacin is a safe, effective method of tocolysis in patients with advanced cervical dilation.
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Hypoxia-ischemia produces brain damage by processes that continue for many hours after reoxygenation/reperfusion. This provides a window of opportunity for therapy aimed at preventing further loss of brain cells. Sulfate magnesium can prevent posthypoxic brain injury by blocking glutamate receptors within the calcium (Ca++) ion channel. We used sulfate magnesium in nine newborn infant after perinatal hypoxia. We investigated the brain damage, by ultrasound examination, on third day, in first, second and third week, and third, sixth month of life. We have estimated the neurological development in the first week of life and third and twelfth month of life. We did not find deviations in ultrasound examination. We did not observe convulsions. We did not observe any side effect of this therapy. The examination at 1 of year of life in all of children was correct.
The purpose of this investigation was to determine the suitability of orally administered magnesium sulfate as a source of inorganic sulfate for counteracting the systemic depletion of sulfate caused by large doses of acetaminophen and certain other drugs that are metabolized to sulfate conjugates. Oral administration of 13.9 g magnesium sulfate U.S.P., in 4 equal hourly increments, to seven healthy men resulted in the urinary excretion (corrected for baseline excretion rate) of an amount of inorganic sulfate equivalent to 30.2 +/- 17.2 percent (mean +/- SD) of the dose during the first 24 hours. Excretion during the subsequent 48 hours was negligible. Six of the subjects experienced loose stools or diarrhea. Compared to sodium sulfate, magnesium sulfate appears to be absorbed less completely and more erratically, and to produce more adverse effects.
Magnesium sulfate was administered intravenously (0.6 mEq/kg body weight over 10 min) to 13 patients with hypertrophic cardiomyopathy undergoing electrophysiologic testing. Total serum, ultrafilterable and protein-bound serum, mononuclear blood cell (MBC) content and concentration, and red blood cell (RBC) concentration of Mg were measured at the following intervals: (1) baseline (before Mg infusion), (2) at the end of infusion, and (3) approximately 40 min after the end of infusion. The total serum, ultrafilterable, and protein-bound fractions rose immediately after infusion and fell by 40 min. The RBC Mg rose and fell less sharply than the serum parameters after Mg infusion. In contrast, the MBC Mg content continued to rise significantly at 40 min after Mg infusion, and MBC concentration showed a continued trend to rise, although this was not statistically significant.
Water-miscible solvents, such as acetone and acetonitrile, effectively extract both polar and nonpolar pesticide residues from nonfatty foods. The addition of sodium chloride to the resulting acetonitrile-water or acetone-water extract (salting out) results in the separation of the water from the organic solvent. However, the organic solvent layer (pesticide extract) still contains some residual water, which can adversely affect separation procedures that follow, such as solid-phase extraction and/or gas chromatography. Drying agents, such as sodium sulfate or magnesium sulfate, are used to remove the water from the organic extracts. In the present study, we used nuclear magnetic resonance spectroscopy to study the composition of the phases resulting from salting out and to compare the effectiveness of sodium sulfate and magnesium sulfate as drying agents. The study showed that considerable amounts of water remained in the organic phase after phase separation. Sodium sulfate was a relatively ineffective drying agent, removing little or no residual water from the organic solvent. Magnesium sulfate proved to be a much more effective drying agent.
BACKGROUND: Magnesium sulfate continues to be widely used as a tocolytic agent despite a paucity of evidence supporting its use. Many practitioners use prolonged courses of magnesium sulfate, sometimes for months. This study was conducted to determine maternal and neonatal outcome of patients exposed to prolonged tocolytic magnesium sulfate. METHODS: A retrospective review of maternal and neonatal charts (1995-2003) of pregnancies that received tocolytic magnesium sulfate. Cases who received magnesium sulfate >48 h (n=78) were compared to controls who received it < or =48 h (n=77) for maternal side effects and neonatal outcome. RESULTS: Cases were more likely to be nulliparous (55.1% versus 37.7%, p=0.044), multiple gestations (33.3% versus 10.4%, p=0.001), and of lower gestational age (29.0+/-3.9 versus 30.5+/-3.8 weeks, p=0.017) compared to controls. The median magnesium sulfate infused was 154 (78-5,500) versus 54 (8-86) g (p<0.001) and the highest maternal magnesium level was 6.5+/-1.7 versus 5.6+/-1.9 mg/dl (p=0.002) in cases and controls, respectively. Cases were more likely to have > or =1 adverse side effect (30.8% versus 15.6%, p=0.045). The median neonatal magnesium level was significantly higher in cases (3.3 (1.4-7.2) versus 2.6 (1.1-5.2) mg/dl, p=0.016); however, neonatal mortality and other neonatal morbidity rates were similar in both groups. Abnormal bone mineralization was encountered in 3 neonates (cases). CONCLUSIONS: Maternal morbidity rate is higher with prolonged intake of tocolytic magnesium sulfate compared to < or =48-h regimen. Despite similar neonatal morbidity and mortality rates, bone demineralization in the neonates may be encountered.
The frequency of blood samples that achieved therapeutic level was lower in the group of maintenance with intravenous regimen than the intramuscular regimen significantly at 15, 30, 60, 120 and 240 minutes after loading dose. The mean level of serum magnesium sulfate in the intravenous group was significantly lower than intramuscular group. This study supported to choose the maintenance by intramuscular regimen. However, further study is required to analyse the effect of higher level of magnesium sulfate in Thai patients.
Time courses of equilibration for three salts, sodium chloride, ammonium sulfate and magnesium sulfate heptahydrate have been measured in the Z/3 crystallization plate. It is shown that by varying both the diffusant and the reservoir depth the time taken to equilibrate can be as short as 200 or as long as 1400 h. Thus, the present design of the plate should accommodate a wide variety of desired crystallization kinetics.
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Magnesium sulfate has attracted interest as a potential neuroprotectant but passage of magnesium ion into the central nervous system has not been well documented. For this study, we quantified plasma and cerebrospinal fluid (CSF) ionized magnesium concentration after systemic magnesium sulfate infusion in patients with intracranial hypertension. Patients ( N = 9) received an intravenous infusion of 5 g/20 mmol magnesium sulfate (125 mL of a 4% wt/vol solution) over 30 minutes. Before and after dosing, CSF (from an indwelling ventricular catheter) and blood samples were collected at hourly intervals. Ionized magnesium concentration in all samples was determined using an electrolyte analyzer. Baseline plasma and CSF ionized magnesium concentrations were 0.58 +/- 0.05 and 0.82 +/- 0.06 mmol/L, respectively. Intravenous magnesium sulfate infusion significantly increased plasma ionized magnesium concentration (peak, 0.89 +/- 0.11 mmol/L), but CSF magnesium levels did not change during the 4-hour study. Systemic administration of magnesium sulfate failed to increase CSF ionized magnesium concentration in patients with intracranial hypertension despite increasing plasma magnesium levels by >50%.