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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fusarium moniliforme was cultured semicontinuously on a carob medium in a 14-liter fermentor (8.5-liter working volume). The growth medium provided 2.4% carob sugar, 0.72% NH4H2PO4, and 0.03% MgSO4-7H2O. The biomass harvest was 8.8 g/liter per day. Ninety percent of the sugars were consumed, and the pH dropped from 5.9 to about 3.7. The crude protein (N X 6.25) of the spray-dried mycelium was 380 g/kg, 300 g/kg for the true protein (Lowry), and 4.8 g/kg for the (Folin-Denis) tannic acid. The mycelium was evaluated nutritionally with the weanling rat as experimental animal. The protein efficiency ratio and net protein utilization values for the unsupplemented mycelium were 1.15 and 0.42, respectively, and for the mycelium supplemented with DL-methionine (5 g/kg) they were 2.31 and 0.72, respectively. No growth depression was observed in the experimental rats, and on dissection of the carcasses the internal organs were found to be normal.
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PMID:Growth of Fusarium moniliforme on carob aqueous extract and nutritional evaluation of its biomass. 0 52

Total content of water, extracellular spaces (ES), na+, K+, and C1- in the isolated chick retina were measured in the presence (test) or absence (control) of spreading depression (SD). During SD in medium with 0.5 mM or 2 mM MgSO4, there is an increase in the intracellular concentration of Na+ and C1- and a decrease in the intracellular concentration of K+. A decrease in the ES was only found in the medium with 2 mM MgSO4 together with a diminished outmovement of K+. We suggest that a decrease in the ES is due to an increased absorption of K+ by the Muller cells, causing its swelling and consequently a decrease of the ES. The addition of sucrose (17 mM) to the incubation medium as the extracellular marker markedly decreased the intracellular concentration of C1- in control retinas, blocked the inward movement of this ion to the tissue during SD and also changed the K+ movement during the phenomenon in medium with 2 mM MgSO4. We suggest that C1- is an important ion in the ionic balance of the Muller cells and that sucrose must have its site of action at these cells.
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PMID:Changes in fluid compartments and ionic composition in the isolated chick retina during SD. 45 Jan 74

The purpose of this study was to investigate whether magnesium sulfate (MgSO4) at a dose commonly used to treat arrhythmias potentiates vecuronium. After Institutional Review Board approval, 20 randomly assigned, consenting patients received a bolus of either MgSO4 (30 mg/kg) or placebo in a blinded fashion. Immediately after receiving the bolus of either MgSO4 or placebo, the study patients were taken to the operating room (OR) and anesthetized. The ED95 of vecuronium was determined in both groups by administering 10 micrograms/kg boluses of vecuronium until 95% twitch depression was measured. Delay to 25% twitch height recovery (indicating that the neuromuscular block could be reversed for extubation) was measured in 10 patients. Ultrafilterable magnesium levels were measured in a total of 13 patients. Magnesium levels were drawn before the magnesium/placebo bolus, 5 minutes after bolus, and 30 minutes after bolus. The data did not demonstrate any relationship between the use of MgSO4 at 30 mg/kg doses and either the ED95 or the duration of vecuronium. A 30 mg/kg bolus of MgSO4 roughly doubled ultrafilterable magnesium levels from baseline. The limited sample size precluded making any firm conclusions from this data. The data trend suggested that antiarrhythmic doses of MgSO4 may not potentiate vecuronium.
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PMID:Do antiarrhythmic doses of magnesium potentiate vecuronium? 134 37

Although alcohol has long been known to induce cardiac depression and cardiomyopathy, it is not known whether drug therapy or pharmacologic manipulation can be used to prevent or reverse these toxicities. With this in mind, high levels (15 mM) of magnesium (Mg) were investigated for their potential antialcohol effects on perfused rat hearts. A high concentration of ethanol (135 mM) was used to induce rapid cardiac failure as assessed by hemodynamic and metabolic parameters. During ethanol perfusion in normal 1.2 mM [Mg2+]o physiologic salt solution, coronary flow decreased immediately, and all of the hemodynamic parameters studied (except for heart rate) were depressed significantly. After 10 min of 135 mM ethanol perfusion, only 60% of the hearts kept beating; at 15 min, only 42% of the hearts continued to beat. Myocardial metabolism under such conditions as assessed by examination of coronary effluent concentrations of lactic acid (LA), lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) was rapidly and severely compromised. Although 15 mM MgSO4 alone did not alter coronary flow and systolic pressure under the conditions studied, it did decrease cardiac output, heart rate and total pressure developed. However, when 15 mM MgSO4 was given 10 min before ethanol, and continued during ethanol perfusion, the usual depression in all assessed cardiac hemodynamic parameters (except heart rate) caused by ethanol was not observed. During 15 min of high [Mg2+]o perfusion, coronary flow recovered from 19.1 +/- 6.8% (ethanol alone) to 68.1 +/- 9.9% of control values (p < 0.01); cardiac output recovered from 10.4 +/- 4.6% (ethanol alone) to 43.6 +/- 7.5% of control (p < 0.01); stroke volume went from 12.9 +/- 5.8% (ethanol alone) to 97.1 +/- 14.5% of control (p < 0.01); systolic pressure from 55.3 +/- 3.6% (ethanol alone) to 88.8 +/- 4.0% of control (p < 0.01), and total pressure developed from 23.9 +/- 7.8% (ethanol alone) to 35.0 +/- 4.5% of control (p < 0.05). Assessment of the metabolic biochemical parameters supported these changes in hemodynamic improvement. For example, LA, LDH and CPK all went from elevated values towards normal levels. There were similar hemodynamic and metabolic responses to high [Mg2+]o given during ethanol perfusion to that given before ethanol perfusion. The hemodynamic and metabolic beneficial effects between groups pretreated or treated with high [Mg2+]o exhibited no significant differences. These results suggest that high [Mg2+]o (15 mM) given either before or during ethanol-induced cardiotoxicity is effective in attenuating both functional and metabolic damage caused by high ethanol perfusion in the rat heart.
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PMID:Beneficial effects of high magnesium on alcohol-induced cardiac failure. 166 23

The effect of acutely elevated serum magnesium on the CNS and cardiac toxicity of bupivacaine was studied. Anesthesia was induced in mongrel dogs with thiopental, 25 mg/kg, and ventilation was controlled. Sedation was maintained with fentanyl (25 micrograms/kg bolus and 5 micrograms.kg-1h-1) and pancuronium (0.15 mg/kg bolus and 0.05 mg.kg-1h-1) provided paralysis. Two hours after the thiopental bolus, all animals received an intravenous (iv) infusion of bupivacaine (1 mg.kg-1 min-1). The control group (5 animals) received bupivacaine only. The Mg++ group (5 animals) received MgSO4 140 mg/kg iv and 80 mg.kg-1 h-1 15 min prior to beginning the bupivacaine infusion. Lead II ECG, cardiac hemodynamics, and two-channel EEG were continuously monitored. Serum magnesium concentrations in the Mg++ group rose from 0.67 mM (1.3 mEq/L) to 2.42 mM (4.8 mEq/L). The bupivacaine infusion caused PR and QRS interval prolongation in both groups, but QRS widening was greater in the control group. QT interval corrected for heart rate (QTIc) lengthened only in the control group. A depression of left ventricular stroke work index (LVSWI) occurred to an equal extent in both groups. The seizure dose of bupivacaine was not different between the two groups: 12.9 +/- 2.3 (SEM) mg/kg in the control group and 13.9 +/- 2.5 mg/kg in the Mg++ group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of magnesium sulfate administration on cerebral and cardiac toxicity of bupivacaine in dogs. 230 66

A transient increase in extracellular calcium concentration causes a long-lasting enhancement of radiatum fibers evoked excitatory postsynaptic potential and population spike responses of CA1 pyramidal neurons which resembles long-term potentiation (LTP). The duration of this potentiation is much longer than described previously and is probably limited by the survival of the preparation itself (greater than 8 hr). Therefore, Ca-induced LTP can be used for the investigation of a postulated late phase of LTP. Ca effects were activity-independent, since the subsequently evoked responses were facilitated even when the presynaptic fibers were not concurrently stimulated during or immediately after superfusion with the high Ca medium. In contrast, if too frequent testing of the synaptic input was done during the high Ca pulse, a short lasting depression instead of potentiation was observed. A lower extracellular magnesium concentration in the standard medium (1.3 instead of 2.0 mM MgSO4) prevents the potentiation of the EPSP at least for the first few hours. Presumably, both tetanus- and Ca-induced LTP share some common mechanisms, since an additional tetanization after Ca induction was not followed by an additional LTP. Compared to the potentiation following tetanization, the Ca-induced LTP was, however, not accompanied by a potentiation of the EPSP/spike ratio within the range of the population spike threshold intensity.
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PMID:Calcium-induced long-term potentiation in the hippocampal slice: characterization of the time course and conditions. 302 Dec 91

The effect of metabolic inhibitor, hypothermia (4 degrees C) and hyperbaric oxygenation (3 atm) on prolonging survival of the canine anoxic heart has been evaluated. Donor hearts were obtained from small mongrel dogs by giving the pre-cooled perfusate of 2 per cent magnesium sulfate (MgSO4), 5 per cent low molecular weight dextran (LMWD) and 2 per cent glucose into the right atrium. Excised hearts were kept at 4 degrees C in a hyperbaric chamber pressurized to 3 atm. After 18 to 48 hours the preserved hearts were transplanted to the neck of recipients by the methods of Marcus. The viability of the preserved hearts were evaluated with functional, biochemical and histologic parameters. Of 29 hearts preserved for 18 to 36 hours, 27 hearts returned to a strong coordinated beat and could maintain function for over 4 hours. Of 5 hearts preserved for 48 hours, 4 showed a coordinated ventricular beat, however, failed to maintain cardiac work over 4 hours. The hearts with 18 to 36 hours storage showed no significant abnormalities on myocardial metabolism and morphology as compared to the control group of the immediately transplanted hearts. The protective action of magnesium is probably related to a number of factors, including metabolic depression and stabilizing effect on membrane permeability of cells to potassium, which would tend to maintain a more normal membrane potential and sub-cellular particles. These studies indicate that viability of the mammalian anoxic hearts can be extended to 36 hours by the combined use of metabolic blockade, hypothermia and hyperbaria suggesting a practical approach to procurement and preservation of cadaver organs.
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PMID:Heart preservation with metabolic inhibitor, hypothermia, and hyperbaric oxygenation. 461 84

In order to study the neuromuscular interactions between suxamethonium and magnesium sulphate (MgSO4), we have determined the dose-response relationship of suxamethonium and the neuromuscular actions of 1.25 x ED50 dose of suxamethonium, both before and after pretreatment with MgSO4. We have also compared the effect of 1.25 x ED50 dose of suxamethonium in the absence and in the presence of 50% neuromuscular block, established previously by infusion of MgSO4. Twenty-one cats were anaesthetized with urethane. Train-of-four stimulation was applied every 12 s to the sciatic nerve and the force of contraction of the tibialis anterior muscle was measured. The potency of suxamethonium decreased in each instance with pretreatment with MgSO4. The ED50 of suxamethonium increased significantly from mean 21.0 (SEM 1.9) micrograms kg-1 before MgSO4 to 25.6 (2.3) micrograms kg-1 after MgSO4 60 mg kg-1 and to 26.6 (2.2) micrograms kg-1 after MgSO4 90 mg kg-1 (P < 0.05). Twitch depression produced by 1.25 x ED50 dose of suxamethonium decreased significantly with MgSO4 pretreatment, from 76.7 (2.6)% before MgSO4 to 61.7 (6.4)% after MgSO4 60 mg kg-1 and 48.7 (7.5)% after MgSO4 90 mg kg-1 (P < 0.05). With stable 50% neuromuscular block, established previously by infusion of MgSO4, the 1.25 x ED50 dose of suxamethonium produced more twitch augmentation (133 (6.3)% vs 108.3 (1.3)%; P < 0.05) and less twitch depression (31.6 (9.6)% vs 74.1 (0.6)%, P < 0.05) than in the absence of MgSO4. The results of all three methods demonstrated that the pharmacological interaction between suxamethonium and magnesium was antagonistic.
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PMID:Neuromuscular interactions between suxamethonium and magnesium sulphate in the cat. 802 15

1. Previous work has suggested that presynaptic effects of adenosine may be dependent on divalent cations. The present study was undertaken to determine whether a similar requirement existed at postsynaptic sites. 2. Extracellular recordings were made in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum or antidromic stimulation of the alveus. In antidromic stimulation experiments, CaCl2 was omitted (calcium-free medium) or reduced to 0.24 mM (low calcium medium) and in some experiments MgSO4 was increased to 2 mM. Kynurenic acid at concentrations of 1 and 5 mM in calcium-free medium and 1 mM in low calcium medium had no effect on secondary spike size. 3. Adenosine and baclofen induced a concentration-dependent reduction in the amplitude of orthodromic potentials with maximum effects at 20 and 5 microM respectively. 4. In nominally calcium-free medium, bursts of multiple population spikes were obtained in response to antidromic stimulation. Adenosine had little effect in reducing the secondary spike amplitude. At high concentration (2 mM) an initial depression was seen which declined within 3-5 min. 5. Sensitivity to adenosine was restored in low calcium medium or by raising magnesium. Although raising the divalent cation concentration increased the inhibitory effect of adenosine, desensitization was still seen. 6. 2-Chloroadenosine (100-500 microM) and R-PIA (50 microM), which are not substrates for either the nucleoside transporters or adenosine deaminase, were inactive in the absence of calcium. S-(2-hydroxy-5 nitrobenzyl)-6-thioinosine, an adenosine uptake blocker, at a concentration 100 MicroM had no effect on secondary potential size and did not restore adenosine sensitivity in calcium-free medium.7. Thapsigargin, which discharges intracellular calcium stores, had no significant effect at 1 MicroM on the bursts of action potentials and did not change the effect of 0.5 mM adenosine in calcium-free medium.8. Unlike adenosine, baclofen concentration-dependently reduced the secondary spike size in calcium free medium and no sign of recovery was observed during maintained superfusion for up to 45 min. No cross-desensitization was seen between baclofen and adenosine.9. Applications of adenosine locally by pressure to neuronal somata or dendrites still resulted in desensitized responses in calcium-free medium.10. It is concluded that the postsynaptic sensitivity to adenosine is dependent on the concentration of divalent cations in the extracellular space implying an effect of cations on adenosine receptor activation or transduction processes.
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PMID:The effect of calcium removal on the suppression by adenosine of epileptiform activity in the hippocampus: demonstration of desensitization. 803 57

Effects of magnesium (Mg) on muscle compound action potentials (CAPs) which were elicited from gastrocunemius muscle by sciatic nerve stimulation in cats were studied, and the results were compared with those of alpha-bungarotoxin (alpha BuTX) and of non-depolarizing relaxants which had been reported previously. Recovery curves (RCs) of CAPs and train-of-four ratios (TOFR) as parameters of neuromuscular blockade were estimated during blocks by Mg as well as the methods described in the previous reports. The following results were obtained. 1) Neuromuscular blocks which were dependent on serum [Mg2+] were observed in accordance with cumulative dosages of MgSO4 solutions. 2) Recovery curves of CAPs showed a pattern which was characterized by extreme potentiations of test responses at shorter intervals of paired stimuli, followed by a slight depression at longer intervals than 500 msec. This pattern of RC was remarkably different from those after alpha BuTX and relaxants. 3) The mechanisms to produce these differences of RCs were discussed, and it is concluded that the notable depression of RCs derived from muscle relaxants may be caused by inhibitory effect on nerve terminals of relaxants which have different mechanism from that by Mg.
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PMID:[Study of neuromuscular transmission with evoked electromyography--11. Comparison between blocks by magnesium and by pancuronium]. 818 19


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