Magnesium sulfate increases the rate of hypothermia via surface cooling and improves comfort.
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BACKGROUND AND PURPOSE: Therapeutic hypothermia shows promise as a treatment for acute stroke. Surface cooling techniques are being developed but, although noninvasive, they typically achieve slower cooling rates than endovascular methods. We assessed the hypothesis that the addition of intravenous MgSO4 to an antishivering pharmacological regimen increases the cooling rate when using a surface cooling technique. METHODS: Twenty-two healthy volunteers were studied. Hypothermia was induced using a surface technique with a target tympanic temperature (Ttym) of 34.5 degrees C (target range 34 to 35 degrees C). Subjects received 1 of the following pharmacological regimens: (1) meperidine monotherapy (n=5); (2) meperidine plus buspirone, 30 to 60 mg PO administered at the time of initiation of cooling (n=4); (3) meperidine and ondansetron, 8 to 16 mg IV administered as an 8 mg bolus at the time of initiation of cooling with an optional second dose after 4 hours as needed for nausea (n=5); or (4) meperidine, ondansetron, and MgSO4, 4 to 6 g IV bolus followed by 1 to 3 g per hour infusion (n=8). Thermal comfort was evaluated with a 100-mm-long visual analog scale. RESULTS: More subjects who received MgSO4 were vasodilated during hypothermia induction (7 of 8 [88%] versus 4 of 14 [29%]; P=0.024). MgSO4 (coefficient -17.265; P=0.039), weight (1.838, 0.001), and the initial 2-hour meperidine dose (0.726, 0.003) were found to significantly impact the time to achieve Ttym of 35 degrees C. Subjects who received MgSO(4) had significantly higher mean comfort scores than those who did not (48+/-15 versus 38+/-12; P<0.001). CONCLUSIONS: Administration of intravenous MgSO(4) increases the cooling rate and comfort when using a surface cooling technique. (+info)
Best evidence topic report. Nebulised magnesium in asthma.
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A short cut review was carried out to establish whether the addition of nebulised magnesium sulphate to beta agonist therapy improves outcome in acute asthma. Altogether 69 papers were found using the reported search, of which five presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these best papers are tabulated. A clinical bottom line is stated. (+info)
Treatment of severe persistent pulmonary hypertension of the newborn with magnesium sulphate.
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Eight of nine newborn infants with severe persistent pulmonary hypertension of the newborn (PPHN), and a predicted mortality of 100%, and one infant with a predicted mortality greater than 94% based on alveolar-arterial oxygen tension difference [A-a)DO2) were treated with magnesium sulphate (MgSO4) as a life saving therapy after they failed to improve with conventional treatment. Magnesium at high serum concentrations decreases pulmonary pressures and is a muscle relaxant and sedative. Diluted MgSO4.7H2O solution (200 mg/kg) was given intravenously over 20-30 minutes. No changes in the treatment were made after MgSO4. Mean serum magnesium concentration was maintained between 2.88 and 5.67 mmol/l by continuous intravenous infusion (six infants). Baseline arterial oxygen tension (PaO2) and haemoglobin oxygen saturation had mean (SD) values of 4.66 (1.8) kPa and 60.4 (29.7)% respectively, which started to increase one hour after MgSO4 infusion, and increased significantly at six hours to 12.04 (7.07) kPa and 91.8 (10.88)% respectively. Arterial carbon dioxide tension (PaCO2) decreased and pH increased significantly after one hour compared with the baseline value. PaO2 increases are probably secondary to a decrease in pulmonary vascular resistance and pressure, decrease in a right to left shunt, better ventilation:perfusion ratio, and PaCO2 decrease and pH rise. Seven infants survived (77.8%). These results demonstrate the beneficial effect of magnesium in the management of PPHN when other accepted treatment fails, is contraindicated, or not available. (+info)
Magnesium inhibits norepinephrine release by blocking N-type calcium channels at peripheral sympathetic nerve endings.
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Although Mg2+ contributes to blood pressure regulation partly in terms of vasodilator action, its sympatholytic effect may also play an important role to control blood pressure. Thus, in the present study, we investigated the effect of Mg2+ on sympathetic tone and blood pressure. We studied its actions on the blood pressure response to hydralazine, a direct vasodilator, in conscious spontaneously hypertensive rats (SHRs), and to electrical stimulation in the pithed Sprague-Dawley rat; catecholamine release by peripheral sympathetic nerve endings; and the N-type Ca2+ channels of cultured neural cells. Intravenous Mg2+ infusion (MgSO4: 3x10(-6) mol/kg body weight/min) induced the greater hypotensive response to hydralazine with attenuated reflex tachycardia in SHRs. In pithed rats, Mg2+ infusion significantly attenuated the blood pressure elevation (2+/-2 mm Hg versus 27+/-6 mm Hg, P<0.01) in response to spinal electrical stimulation. In the perfused mesenteric arteries system, norepinephrine release was significantly attenuated (51+/-2%, P<0.01) by high Mg2+ concentration solution (4.8 mmol/L) compared with normal Mg2+ solution (1.2 mmol/L). When we applied the perforated whole-cell patch clamp method to nerve growth factor-treated PC12 cells, Mg2+ blocked voltage-gated Ca2+ currents in a concentration-dependent manner. The majority of the voltage-gated Ca2+ currents were carried through N-type channels, followed by L-type channels. Mg2+ blocked both of these channels. These findings suggest that Mg2+ blocks mainly N-type Ca2+ channels at nerve endings, and thus inhibits norepinephrine release, which decreases blood pressure independent of its direct vasodilating action. (+info)
Influence of magnesium sulphate on evoked activity of rat brain after exposure to short-term hypoxia.
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Young Wistar rats (aged 12, 25 and 35 days) were exposed to short-term (60 min) hypobaric hypoxia of 41 kPa. Cortical afterdischarges (ADs) were evoked by repeated direct stimulation of the sensorimotor cortex and the duration of ADs was monitored to examine the influence of magnesium sulphate injection (0.3 g/kg b.w.). In 12-day-old hypoxia-exposed rats, an increase of the mean duration of ADs after the repeated stimulation appeared. This effect was prevented by magnesium administration. In 25- and 35-day-old rats exposed to hypoxia a shortening of ADs was registered but no specific effect of magnesium sulphate pretreatment was observed. The brain susceptibility and ability to terminate evoked seizures is discussed. (+info)
Resistance artery vasodilation to magnesium sulfate during pregnancy and the postpartum state.
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This study compared the vasodilatory responses to magnesium sulfate (MgSO(4)) of cerebral and mesenteric resistance arteries and determined whether the responses varied between different gestational groups. Third-order branches (<200 microm) of the posterior cerebral (PCA) and mesenteric arteries (MA) were dissected from nonpregnant (NP; n = 6), late pregnant (LP; day 19, n = 6), and postpartum (PP; day 3, n = 6) Sprague-Dawley rats. A concentration-response curve was performed by replacing the low-MgSO(4) (1.2 mM) HEPES buffer solution with increasing concentrations of MgSO(4) (4, 6, 8, 16, and 32 mM) and measuring lumen diameter at each concentration. All groups exhibited concentration-dependent dilation to MgSO(4), decreasing the amount of tone in the vessels. However, MA were significantly more sensitive to MgSO(4) than PCA. Whereas there was no difference in the response between different gestational groups in MA, the PCA from the LP and PP groups showed a significantly diminished response to MgSO(4). The percent dilation at 32 mM MgSO(4) for PCA versus MA in NP, LP, and PP animals was 36 +/- 2 vs. 51 +/- 7% (P < 0.05), 19 +/- 9 vs. 54 +/- 6% (P < 0.01 vs. PCA and NP), and 12 +/- 5 vs. 52 +/- 11% (P < 0.01 vs. PCA and NP). These results demonstrate that MgSO(4) is a vasodilator of small resistance arteries in the cerebral and mesenteric vascular beds. The refractory responses of the PCA in LP and PP groups demonstrate changes in the cerebrovascular vasodilatory mechanisms with gestation. The greater sensitivity of the MA to MgSO(4)-induced vasodilation suggests that the prophylactic effect of MgSO(4) on eclamptic seizures may be more closely related to the lowering of systemic blood pressure than to an effect on cerebral blood flow. (+info)
Mineralogy at Meridiani Planum from the Mini-TES Experiment on the Opportunity Rover.
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The Miniature Thermal Emission Spectrometer (Mini-TES) on Opportunity investigated the mineral abundances and compositions of outcrops, rocks, and soils at Meridiani Planum. Coarse crystalline hematite and olivine-rich basaltic sands were observed as predicted from orbital TES spectroscopy. Outcrops of aqueous origin are composed of 15 to 35% by volume magnesium and calcium sulfates [a high-silica component modeled as a combination of glass, feldspar, and sheet silicates (approximately 20 to 30%)], and hematite; only minor jarosite is identified in Mini-TES spectra. Mini-TES spectra show only a hematite signature in the millimeter-sized spherules. Basaltic materials have more plagioclase than pyroxene, contain olivine, and are similar in inferred mineral composition to basalt mapped from orbit. Bounce rock is dominated by clinopyroxene and is close in inferred mineral composition to the basaltic martian meteorites. Bright wind streak material matches global dust. Waterlain rocks covered by unaltered basaltic sands suggest a change from an aqueous environment to one dominated by physical weathering. (+info)
MgSO4 and lazaroid (U-83836E) partially protects glioma cells against glutamate toxicity in vitro.
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In this study, the possible effects of MgSO4 and lazaroid (U-83836E) on glutamate toxicity on glial cells were investigated. C6 and human glioblastoma multiforme cells derived from two patients were grown in an incubator. First, determined IC50 dose of L-glutamate (L-glu) was given for 24 hours and removed, and then respective MgSO4 or U-83836E doses were added to the culture medium. After 24 hours 3-(4,5-Dimethylthyazol-2-yl)-2,5-diphenyltetrazolium bromide, thiazolyl blue (MTT) test was applied. When compared to the L-glu-treated group, MgSO4 at the dose of 0.01 mM induced C6 and human glioma cell growth by 17%, 15% and 5%, respectively. At the dose of 1 microM U-83836E also increased C6 and human glioma cell growth by 12%, 13% and 5%, respectively. In conclusion, although MgSO4 and U-83836E do not strongly block glutamate-induced cell death, it is suggested that reduction of Mg2+ ions and free radical production may have a role in glutamate toxicity on glial cells. (+info)