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Magnesium absorption in mature ewes infused intrarumenally with magnesium chloride.

The effects of magnesium supplementation on Mg absorption proximal and distal to the pylorus in ewes maintained on a grass diet were investigated using a combination of balance, digesta flow and electropotential measurements. Three mature ewes each received by intrarumenal infusion a supplement of 0, 1, 2 and 3 g Mg/d in sequence over four 10-d periods. Net Mg absorption distal to the pylorus took place down its electrochemical gradient, although the quantity absorbed remained small during the control and first infusion periods. The bulk of Mg absorption occurred before the pylorus and, during the control and first infusion periods, took place against its electrochemical gradient. The net Mg absorption proximal to the pylorus rose with declining efficiency as Mg intake was increased. It is suggested that saturation of the absorption process at this site was occurring.

Animals↗

Clastogenicity in vitro of the Na, K, Ca and Mg salts of saccharin; and of magnesium chloride; consideration of significance.

The sodium, potassium, calcium and magnesium salts of saccharin, and magnesium chloride, have been shown to be clastogenic to Chinese hamster lung (CHL) fibroblasts in vitro, but only at elevated dose levels (8-16 mg/ml). Saccharin acid was inactive to the limits of its solubility (4 mg/ml). When the data are expressed in terms of ionic concentration, each salt showed a similar clastogenic potency. This suggests that ionic effects induced by these salts in the assay medium may be the critical determinant of the clastogenic effects seen, rather than that the saccharin moiety presents a genotoxic insult to the chromosomes of the cells. The metal-chelating agents EDTA and EGTA were non-clastogenic, but the disodium salt of EDTA showed weak activity prior to toxicity at 0.5 mg/ml. The absence of a clastogenic response for the salts of saccharin at dose levels lower than 4 mg/ml is discussed within the context of the threshold-dependent tumour-promoting activity of high dose levels of sodium saccharin to the bladder of male rats. The doubtful value of conducting in vitro clastogenicity studies at dose levels greater than 10(-2) M is discussed.

Animals↗

NMDA receptor blockade in chronic neuropathic pain: a comparison of ketamine and magnesium chloride.

Ten patients (4 female, 6 male) aged 34-67 years suffering from peripheral neuropathic pain participated in a double-blind placebo-controlled study where ketamine or magnesium chloride were administered by a 10 min bolus infusion (ketamine: 0.84 mumol/kg = 0.2 mg/kg, magnesium: 0.16 mmol/kg) followed by a continuous infusion (ketamine: 1.3 mumol/kg/h = 0.3 mg/kg/h, magnesium: 0.16 mmol/kg/h). Ongoing pain determined by VAS score, area of touch-evoked allodynia, detection and pain thresholds to mechanical and thermal stimuli were measured before and during drug infusion. Ketamine produced a significant reduction of spontaneous pain (57%) and of the area of allodynia (33%). Magnesium chloride reduced pain (29%) and area of allodynia (18%) insignificantly. Following ketamine there was a significant correlation between the reduction in ongoing pain and reduction in area of touch-evoked allodynia. Detection and pain thresholds to mechanical and thermal stimuli were not significantly changed by the drugs. These findings suggest that both ongoing pain and touch-evoked pain (allodynia) in neuropathic pain are inter-related phenomena, which may be mediated by the same mechanism and involving a N-methyl-D-aspartate receptor.

Adult↗

Atherogenesis inhibition induced by magnesium-chloride fortification of drinking water.

Magnesium (Mg) modulates blood lipid levels, atherogenesis, and atherosclerosis in rabbits, when supplemented to diet. We have recently reported that a high concentration (50 g/L) of Mg sulfate fortification of drinking water attenuates atherogenesis in male and female LDL-receptor-deficient mice fed a high-cholesterol diet. The aims of the current study were to examine whether lower concentrations and another Mg salt could also have such an antiatherogenic effect. Thirty male LDL-receptor-deficient mice were divided into three groups (n=10 in each group). The mice received either distilled water or water fortified with 0.83 g or with 8.3 g Mg-chloride per liter. In the first (27 wk) and second (5 wk) stages of the experiment, the mice received normal chow and Western-type diet, respectively. Blood was drawn for determination of plasma Mg, calcium, and lipid levels. The extent of atherosclerotic lesions was determined at the aortic sinus. Magnesium-chloride fortification of drinking water did not result in higher plasma Mg concentrations, whereas a trend toward lower plasma calcium concentrations did not reach statistical significance. Even though plasma lipid levels were similar at the beginning and the end of the study, there were decreased plasma cholesterol and triglyceride levels in the Mg groups after stage I. The atherosclerosis extent at the aortic sinus was significantly decreased in the 8.3-g Mg-chloride/L group (23,437 +/- 10,083 micron2) compared with the control group (65,937 +/- 31,761 microm2). There was also a trend toward lower atherosclerosis extent at the aortic sinus in the 0.83-g Mg-chloride/L group. An additional Mg salt (Mg-chloride) fortification of drinking water is capable of inhibiting atherogenesis in male LDL-receptor-deficient mice. That is done in a lower concentration of Mg than previously reported.

Animals↗

The effect of potassium phosphate, magnesium chloride and T6 as blocking reagents on tissue valve calcification.

Potassium phosphate, Magnesium chloride and T6 as blocking agents on tissue valve calcification have been studied in vitro and in vivo. In vitro tests indicate that untreated leaflets (control group) tend to calcify significantly more than treated leaflets (p less than 0.05). Calcification in the treated leaflets tends to be varied with no significant difference (p greater than 0.05) between the different groups. In vivo findings indicate that leaflets in the control group calcify as early as 5 weeks after implantation while treated leaflets showed no significant signs of calcification at this stage. Results deduced from the extractable calcium contents as well as from histological examination, emphasise the need of a blocking reagent to decrease calcification on a valvular bioprosthesis.

Animals↗

Effects of magnesium chloride on cardiovascular hemodynamics in the neurally intact dog.

To assess the cardiovascular actions of magnesium in neurally intact animals, magnesium chloride (1-4 mM/min) administered i.v., producing a peak arterial magnesium level between 4.7 and 7.2 mg/dl, was given to alpha-chloralose-anesthetized, open-chest dogs. Magnesium lowered heart rate by 36 +/- 11 beats/min (P less than .05), cardiac output by 0.7 +/- 0.2 liters/min (P less than .05), left ventricular (LV) peak dP/dt by 410 +/- 96 mm Hg/sec (P less than .05) and aortic and pulmonary artery pressures, but it did not change LV end-diastolic pressure, systemic resistance or pulmonary resistance. Coronary blood flow also decreased by 39 +/- 11% (P less than .05), myocardial oxygen consumption by 88 +/- 22% (P less than .05) and myocardial oxygen extraction by 53 +/- 16% (P less than .05). When heart rate was held constant, magnesium still decreased LV systolic pressure, LV peak dP/dt and coronary blood flow. The increase in serum magnesium was accompanied by an increase in serum calcium (by 1.4 +/- 0.2 mg/dl; P less than .05) and a fall in serum potassium (by 0.21 +/- 0.1 mEq/l), but not by a change in serum sodium, myocardial electrolyte arteriovenous differences or arterial pH. Thus, at blood concentrations that are observed in humans after therapeutic dosages of magnesium, a depression of cardiac performance is observed in the anesthetized dog. Although magnesium produces a fall in coronary blood flow, this appears to be due at least in part to a decrease in myocardial oxygen requirements because myocardial oxygen extraction also decreases. Rapid changes in serum electrolytes accompany these hemodynamic effects.

Animals↗

[Enzyme diagnosis in lipaemic sera before and after polyanion precipitation with heparin and magnesium chloride (author's transl)].

The method for the determination of enzymic activity in turbid, lipaemic sera, which involves clearing by polyanion precipitation with heparin and magnesium chloride, was critically reviewed. In the diagnosis of diseases of the liver and pancreas, which are frequently associated with hyperlipoproteinaemia, only residual enzyme activities are measured in the cleared serum after polyanion treatment. In the measurement of glutamate dehydrogenase and in the Phadebas test for alpha-amylase, the enzymes are inactivated by treatment with heparin and magnesium chloride. On the other hand, as a result of polyanion precipitation gamma-glutamyl transferase is transferred, together with lipoproteins and chylomicrons, to the lipid-rich supernatant. Acid phosphatase also exhibits only residual activity in cleared serum. The activity of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, leucine arylamidase, cholinesterase, creatine kinase, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase, and the activity of alpha-amylase in the Merckotest are not affected by polyanion treatment of the serum.

Anions↗

The influence of magnesium chloride on blood and urine parameters in calcium oxalate stone patients.

The influence of magnesium chloride on various blood and urine parameters in calcium oxalate stone patients is studied. High dose magnesium therapy was found to increase urinary magnesium concentrations, whereas the oxalic acid concentration is reduced. The experiments support the statements on the role of magnesium in endogenous oxalic acid depression and the inhibition of the intestinal resorption. For urolith prevention it will be necessary to apply high magnesium doses of easily absorbable and well-tolerated medicaments.

Adult↗

The influence of exogenous magnesium chloride on the apparent INR determined with human, rabbit, and bovine thromboplastin reagents.

Magnesium ions can shorten the tissue factor-induced coagulation time. Some blood collection systems with sodium citrate are contaminated with variable amounts of magnesium and influence the results of the prothrombin time (PT) test. The aim of the study was to determine the dose-response relationship between exogenous magnesium chloride added to blood and the PT and the international normalized ratio (INR). Blood specimens from twenty patients on oral anticoagulant therapy were investigated. Four different types of thromboplastin reagents were used: recombinant human, human placenta, rabbit brain, and bovine brain combined with adsorbed bovine plasma. With all four reagents, exogenous magnesium induced a reduction of the apparent INR. Bovine thromboplastin was not as responsive to magnesium as the human and rabbit reagents. The magnitude of the INR deviation induced by 0.1 mmol/l magnesium in the blood was smaller than 10% in all patient samples. At 0.5 mmol/l magnesium in the blood, 10-35% of the patient samples had INR deviations greater than 10%, depending on the thromboplastin reagent used.

Animals↗

Drug actions in preeclampsia: aspirin, but not magnesium chloride or dihydralazine, differentially inhibits cultured human trophoblast release of thromboxane and prostacyclin without affecting angiotensin II, endothelin-1, or leukotriene B4 secretion.

OBJECTIVE: We hypothesized that aspirin Mg++, and dihydralazine affect the release of vasoactive agents from cultured human placental trophoblast. STUDY DESIGN: Cytotrophoblasts isolated from placentas of preterm or term deliveries of 14 healthy control women and 15 preeclamptic women were cultured in Dulbecco's modified Eagle's medium for 5 days in the presence or absence of either 0.1 mmol/L aspirin, 3 mmol/L magnesium chloride, or 136 ng/ ml dihydralazine. Vasoactive substances were quantitated by radioimmunoassay with mean +/- SEM percentage of untreated cells (= 100%) compared by the Mann-Whitney U test and analysis of variance. RESULTS: Aspirin inhibited (p < 0.01) both thromboxane and prostacyclin on days 1 and 2 in culture but not on days 3 to 5 unless the Dulbecco's modified Eagle's medium was supplemented with arachidonic acid. Aspirin inhibition was greater (p < 0.01) for thromboxane in cells cultured 24 hours after preeclamptic pregnancy (preterm 29.9% +/- 6.8%, term 20.1% +/- 5.9%) compared with normal controls (preterm 66.3% +/- 10.6%, term 68.9% +/- 11.6%). Aspirin reduced (p < 0.01) the ratio of thromboxane to prostacyclin in media of cells from preeclampsia (untreated 27.8 +/- 7.2, aspirin 13.3 +/- 4.4), but aspirin had no effect on this ratio in cultures from control normal pregnancies (untreated 6.8 +/- 2.9, aspirin 4.8 +/- 1.1). Neither magnesium chloride nor dihydralazine affected trophoblast prostanoid production, and no drug altered the media levels of angiotensin II, endothelin-1, or leukotriene B4. CONCLUSION: Aspirin selectively inhibits trophoblast prostanoid production. This inhibition depends on the availability of arachidonic acid and the presence or absence of preeclampsia. Magnesium and dihydralazine effects in pregnancy are not related to altered release of trophoblast vasoactive compounds.

Angiotensin II↗

Postinjury treatment with magnesium chloride attenuates cortical damage after traumatic brain injury in rats.

The neuroprotective effect of magnesium chloride (MgCl2), a compound previously demonstrated to improve behavioral and neurochemical outcome in several models of experimental brain injury, was evaluated in the present study. Male Sprague-Dawley rats were anesthetized and subjected to lateral fluid-percussion brain injury of moderate severity (2.5-2.8 atm). A cannula was implanted in the left femoral vein and at 1 h following injury, animals randomly received a 15 min i.v. infusion of either MgCl2 (125 micromol/rat) or saline. A second group of animals received anesthesia, surgery, and either MgCl2 or vehicle to serve as uninjured (sham) controls. Two weeks following brain injury, animals were sacrificed, brains removed, and coronal sections were taken for quantitative analysis of cortical lesion volume and hippocampal CA3 cell counts. Traumatic brain injury resulted in a lesion in the ipsilateral cortex and loss of pyramidal neurons in the CA3 region of the hippocampus in vehicle-treated animals (p < 0.01 vs. uninjured animals). Administration of MgCl2 significantly reduced the injury-induced damage in the cortex (p < 0.01) but did not alter posttraumatic cell loss in the CA3 region of the ipsilateral hippocampus. The present study demonstrates that, in addition to its beneficial effects on behavioral outcome, MgCl2 treatment attenuates cortical histological damage when administered following traumatic brain injury.

Animals↗

Synthesis of 5-bromopyridyl-2-magnesium chloride and its application in the synthesis of functionalized pyridines.

[reaction: see text] The 5-bromopyridyl-2-magnesium chloride (2), which was not accessible previously, was efficiently synthesized for the first time via an iodo-magnesium exchange reaction with 5-bromo-2-iodopyridine (1). This reactive intermediate was allowed to react with a variety of electrophiles to afford a range of useful functionalized pyridine derivatives. Application of this methodology to 5-bromo-2-iodo-3-picoline provided a simple and economical synthesis of a key intermediate for the preparation of Lonafarnib, a potent anticancer agent.

Magnesium Chloride↗

Absorption of magnesium chloride solution in small bowel disease.

The absorption of a magnesium chloride solution has been observed by balance studies in three patients with ileal resections and in one patient with idiopathic steatorrhoea and biliary cirrhosis. All patients were depleted of magnesium because of malabsorption. The mean net absorption of magnesium increased to 4.5, 4.9, 5.8 and 16.4 mmol magnesium per day, when a supply of 25 mmol magnesium was given. The result was encouraging with positive magnesium balances in all patients.

Journal Article↗

Arrhythmia prophylaxis after coronary artery surgery. A randomised controlled trial of intravenous magnesium chloride.

One hundred and thirty patients undergoing elective myocardial revascularisation were randomised to receive an intravenous infusion containing either 50 mmol magnesium chloride or placebo during the first 48 h following surgery. Magnesium was given to 66 patients and a placebo infusion to 64 patients. Postoperative serum magnesium concentrations fell in the placebo group (from 0.83 +/- 0.06 to 0.79 +/- 0.11 mmol/l) but were elevated in the magnesium group (from 0.82 +/- 0.05 to 1.2 +/- 0.25 mmol/l). In total, 35 patients (26.9%) had a supraventricular arrhythmia, of which 11 were in the magnesium group (16.7%) and 24 (37.5%) in the placebo group (P = 0.013). Three patients in the magnesium group had an episode of ventricular fibrillation and three patients in the placebo group had frequent ventricular ectopics. There was one death in the magnesium group associated with a perioperative myocardial infarction. This study shows that intravenous magnesium supplements reduce the incidence of supraventricular arrhythmias following coronary artery surgery.

Aged↗

Improved myocardial recovery from ischemia. Treatment with low-dose adenosine triphosphate-magnesium chloride.

To evaluate the effects of adenosine 5-triphosphate-magnesium chloride (ATP-MgCl2) on myocardial function following ischemia, mongrel dogs were placed on cardiopulmonary bypass with separate coronary perfusion pressures at 80 mm Hg. An intraventricular balloon was used to assess cardiac function as the area under the pressure-volume curve (PV), compliance (C), and cardiac contractility (dP/dT). Control measurements were made of coronary flow (Q), myocardial oxygen consumption and PV, C, and dP/dT. Myocardial ischemia was then induced for 45 minutes, followed by reperfusion (R). In group 1 (n = 5), no ATP-MgCl2 was infused into the coronary perfusion line. In group 2 (n = 5), low-dose ATP-MgCl2 (0.13 mg/min/kg) was infused during the first 30 minutes of reperfusion (R0 to R30), and in group 3 (n = 5), high-dose ATP-MgCl2 (3.2 mg/min/kg) was infused from R0 to R30. Use of ATP-MgCl2 therapy produced marked coronary vasodilation. After 20 minutes of reperfusion (R20), coronary resistance was 81% +/- 12%, 55% +/- 15%, and 31% +/- 3% of control in groups 1, 2, and 3, respectively. The high-dose ATP-MgCl2 (group 3) caused a marked systemic hypotension, but the low-dose ATP-MgCl2 (group 2) did not. After 75 minutes of reperfusion (R75), compliance was decreased in all groups. In groups 1 and 3, both function (PV) and dP/dT were significantly decreased. However, for group 2 (low-dose ATP-MgCl2), function (PV), and dP/dT were not different from the control group, indicating an excellent recovery. Thus, at low doses, ATP-MgCl2 appears to be a promising adjunct to the treatment of the ischemic myocardium.

Adenosine Triphosphate↗

Improved renal function using adenosine triphosphate-magnesium chloride in preservation of canine kidneys subjected to warm ischemia.

Previous studies have shown that adenosine triphosphate-magnesium chloride (ATP-MgCl2) administered after 30 to 60 min of renal ischemia ameliorated the resulting acute renal failure in different species of animals. The purpose of this study was to determine whether addition of ATP-MgCl2 to the perfusate during renal preservation, prior to transplantation, might improve renal function. Dog kidneys were subjected to normothermic ischemia for 35 min, after which they were preserved by pulsatile perfusion for 24 hr at 7 C. The perfusate contained albumin in a balanced electrolyte solution with an without ATP-MgCl2. Following 24 hr of pulsatile perfusion, the kidneys were autotransplanted and renal function was determined 3 days post-transplantation. The results indicated that dog kidneys subjected to ischemia followed by perfusion preservation developed severe oliguric renal failure 3 days after transplantation. However, if ATP-MgCl2 was added to the perfusate, such kidneys demonstrated markedly improved renal function and ATP levels. These results indicate that kidneys which have been subjected to episodes of warm ischemia could be salvaged by addition of ATP-MgCl2 to the perfusate.

Adenosine Triphosphate↗