Magnesium and trace elements (Magnes Trace Elem)

Publisher: American Society for Magnesium Research

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Other titles Magnesium and trace elements
ISSN 1015-3845
OCLC 21400675
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

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    ABSTRACT: The development of fluorescent ion-selective indicators for magnesium has provided valuable tools for measuring second-by-second changes in cytosolic magnesium activity. In the course of establishing appropriate protocols for using one of these indicators, mag-fura-2, to measure magnesium activity in BC3H-1 cells and chick ventricular myocytes, many potential pitfalls and limitations of this technique have been encountered and addressed. These observations are presented for the purpose of providing guidelines regarding the appropriate use of this indicator and on factors influencing the interpretation of resulting data.
    Magnesium and trace elements 01/1993; 10(2-4):142-50.
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    ABSTRACT: The effect of acute ethanol perfusion on the intracellular free magnesium level, intracellular pH, and high energy phosphate levels of isolated adult rat hearts (n = 13) were studied using 31P nuclear magnetic resonance (NMR) spectroscopy. Perfusion with 1% ethanol solution resulted in a 43% decrease in the intracellular free magnesium level in Langendorff perfused rat hearts while intracellular pH was not significantly altered. In most hearts ethanol perfusion also resulted in increased intracellular inorganic phosphate and reduced phosphocreatine and ATP levels, corresponding to a significant reduction in phosphorylation potential. The implications of these results in the pathogenesis of alcohol-induced hypertension are discussed in light of our previous studies on spontaneously hypertensive and normotensive rats which demonstrated a correlation between cardiac free magnesium levels and blood pressure.
    Magnesium and trace elements 01/1993; 10(2-4):136-41.
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    ABSTRACT: Magnesium, the second most abundant intracellular cation, is essential for life. The consequences of deficiency are severest in the smallest and youngest members of each species and may include sudden unexpected death. Magnesium deficiency, usually diagnosed by hypomagnesemia, may be congenital, as in premature infants, infants of magnesium-deficient mothers and infants with intrauterine growth retardation. It may be acquired or caused by low magnesium intake, the use of magnesium-wasting drugs, illness provoking gastrointestinal or renal losses of the mineral, or high metabolic demands imposed by catch-up growth or postsurgical healing. Finally, the deficiency may be conditioned, caused by excessive dietary calcium, phosphorus or protein in relation to dietary magnesium, especially during a period of rapid growth or tissue repair. Magnesium therapy is safe when a low dosage is given with monitoring of plasma or serum magnesium levels, with occasional checking of calcium and potassium levels. A parenteral dose of 0.1 ml/kg/day of 50% magnesium sulfate USP (approx. 0.2 mmol/kg/day or 0.4 mEq/kg/day) may be given for 5 dose days. An oral dose of 1.0 ml of 10% magnesium chloride solution providing 0.5 mmol/kg/day magnesium or 1.0 ml/kg/day of 10% magnesium chloride USP (0.5 mmol/kg/day) or magnesium magonate (Magonate) 1.0 ml/kg/day (0.45 mmol/kg/day) may be given for extended periods; higher doses may be required for malabsorption syndromes. Hypermagnesemia, which usually results from magnesium overdosage or inadequate renal function, is a potential threat to neonates born to magnesium-treated eclamptic mothers. Most show marked improvement after 36 h of conservative management that includes calcium salts and intravenous infusions of glucose and saline, but obtunded neonates may require dialysis.
    Magnesium and trace elements 01/1993; 10(2-4):229-50.
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    ABSTRACT: Red blood (RBC) ionized magnesium (Mg2+) was determined by nuclear magnetic resonance (NMR) in order to assess the usefulness of this technique as an index of magnesium depletion. Twenty-four normal subjects underwent a 3-week low-Mg diet. The RBC Mg2+ fell from 209 +/- 9.8 microM before diet to 162 +/- 9.3 microM at the end of the 3 weeks (p < 0.001). In patient populations, 22 hypomagnesemic hospitalized patients had a significantly lower RBC Mg than normal (146 +/- 7.1 microM, p < 0.002), and 37 outpatients with diabetes mellitus had a mean RBC Mg2+ of 172 +/- 7.1 microM which was also significantly lower than normal (p < 0.001). These data suggest that determination of RBC Mg2+ may be used to reflect intracellular Mg status.
    Magnesium and trace elements 01/1993; 10(2-4):117-21.
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    ABSTRACT: The cellular bioenergetic responses of isolated perfused working rat hearts to alterations in hemodynamic function caused by acute exposure to elevated levels of extracellular magnesium ions ([Mg2+]o) were examined using 31P nuclear magnetic resonance (31P NMR) spectroscopy. Results showed that in hearts working against 90 cm H2O afterload, an increase in [Mg2+]o from 1.2 to 4.8 mM reduced the heart rate by 35%, while coronary flow was increased by 38%. Unexpectedly, despite the pronounced bradycardia, the rate-pressure product was reduced only slightly (from 2.36 x 10(4) to 2.08 x 10(4) mm Hg/min) due to a significant increase (36%) in systolic pressure. In addition, cardiac output actually increased by 23%, owing to a > 100% increase in stroke volume, indicating that the performance of the heart was improved and suggesting that the efficiency of the heart was improved as well. In a separate series of experiments, 31P NMR measurements performed on hearts perfused in the Langendorff mode revealed that elevated levels of [Mg2+]o increase phosphocreatine (PCr) levels by 23% (from 9.2 to 11.3 mM), while Pi levels declined by a corresponding amount. Perfusion of hearts in the working mode with elevated [Mg2+]o was also observed to increase PCr levels from 6.3 to 9.0 mM, while ATP levels declined by 17%. Measurement of the chemical shift difference between Pi and PCr and that between the alpha and beta phosphate resonances of ATP were used to determine intracellular pH and the cytosolic levels of free Mg2+ ([Mg2+]i), respectively. These results showed that acute exposure of hearts, perfused in either the working or Langendorff mode, to increased levels of [Mg2+]o increased intracellular pH by 0.12-0.13 units, while free Mg2+ nearly doubled to a level of 1.1-1.2 mM. The latter observation may suggest that acute variations in the level of [Mg2+]o can influence a multitude of cellular processes requiring Mg2+ as an essential cofactor. Using the above data and assuming equilibrium of the creatine kinase reaction, the levels of ADP, cytosolic phosphorylation potential ([ATP]/[ADP][Pi]) and free energy change from ATP hydrolysis (-delta G/delta E) were also calculated. Results obtained illustrate that in the presence of elevated [Mg2+]o, ADP levels declined by 33-48%, the cytosolic phosphorylation potential increased from 41 to 112 mM-1 and -delta G/delta E increased from 56.7 to 59.3 kJ/mol. These changes are not completely accountable by the known bradycardia and vasodilatory effects of elevated [Mg2+]o and strongly argue for a direct action of [Mg2+]o on the myocyte as well.(ABSTRACT TRUNCATED AT 400 WORDS)
    Magnesium and trace elements 01/1993; 10(2-4):99-116.
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    ABSTRACT: Magnesium has a profound effect on neural excitability; the most characteristic signs and symptoms of Mg deficiency are produced by neural and neuromuscular hyperexcitability. These create a constellation of clinical findings termed tetany syndrome (TS). TS symptoms include muscle spasms, cramps and hyperarousal, hyperventilation and asthenia. Physical signs (Chvostek's, Trousseau's or von Bonsdorff's) and abnormalities of the electromyogram or electroencephalogram can usually be elicited. Signs and symptoms of TS are frequently encountered in clinical practice, especially among patients with functional or stress-related disorders. The role of Mg deficit in TS is suggested by relatively low levels of serum or erythrocyte Mg and by the clinical response to oral Mg salts, which has been demonstrated in controlled studies. Among the more serious neurologic sequelae of TS are migraine attacks, transient ischemic attacks, sensorineural hearing loss and convulsions. Mg deficiency may predispose to hyperventilation and may sensitize the cerebral vasculature to the effects of hypocarbia. Mg deficiency increases susceptibility to the physiologic damage produced by stress, and Mg administration has a protective effect; studies on noise stress and noise-induced hearing loss are taken as an example. In addition, the adrenergic effects of psychological stress induce a shift of Mg from the intracellular to the extracellular space, increasing urinary excretion and eventually depleting body stores. Drugs used in neurology and psychiatry may affect Mg levels in blood and may diminish signs of tetany, making assessment of Mg status more difficult. Pharmacologic use of Mg can decrease neurologic deficit in experimental head trauma, possibly by blockade of N-methyl-D-aspartate receptors. In conjunction with high doses of pyridoxine, Mg salts benefit 40% of patients with autism, possibly by an effect on dopamine metabolism.
    Magnesium and trace elements 01/1993; 10(2-4):287-301.
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    ABSTRACT: The reference system, preanalytical variables, specimen requirements and methodology for determination of magnesium in serum by clinical laboratories are discussed. Most clinical laboratories determine the serum magnesium concentration by colorimetric methods. Four different chromophores (calmagite, methylthymol blue, formazan dye and magon) are commonly used for the determination of serum magnesium on automated instruments by clinical laboratories. The College of American Pathologists Proficiency Testing Survey shows that instruments using the chromophore magon have a larger coefficient of variation among laboratories than most instruments using a different chromophore.
    Magnesium and trace elements 01/1993; 10(2-4):60-6.
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    ABSTRACT: The concentration of free Mg2+ in the matrix of isolated heart mitochondria has been monitored using the fluorescent probe furaptra. The techniques used for loading, calibrating and using furaptra fluorescence to monitor matrix free Mg2+ are described. Furaptra is loaded as the membrane-permeable acetoxymethyl ester which is hydrolyzed to the impermeant acid form by nonspecific esterases. Loading is sufficient in a 20-min period at 25 degrees C to give signals approximately 5-fold greater than nonloaded mitochondria. Uncertainties concerning the apparent dissociation constant value for Mg2+ for entrapped furaptra and the ability of ionophores to equilibrate Mg2+ across the mitochondrial membrane are discussed. We conclude that our best estimate for matrix Mg2+ in isolated mitochondria is 0.5 mM and that it can change significantly with changing Mg2+ ligand availability in the matrix.
    Magnesium and trace elements 01/1993; 10(2-4):151-64.
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    ABSTRACT: The magnesium content of the adult human is approximately 24 g (1 mol), about half lies in bone and half in soft tissue. Less than 1% of the total body magnesium is present in blood, with approximately 0.3% present in serum. Total magnesium has been determined in several body tissues, but we lack information about free magnesium, which has physiologic significance. Current assessment of magnesium status is difficult as there is no simple, rapid and accurate test(s) to indicate total body magnesium status. I discuss 12 tests in three functional categories that have been used clinically or in research to assess magnesium status. Determining total magnesium in tissues and physiologic tests may provide important information. A test for the routine determination of free magnesium in serum should improve the assessment of magnesium status. A combination of available tests is recommended.
    Magnesium and trace elements 01/1993; 10(2-4):172-81.
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    ABSTRACT: Diagnostic categories that are useful for describing patients with acute or organ failure disease are generally less useful labels for primary care and preventive medicine patients whose conditions are better described by signs and symptoms. Symptoms may be clues to ill health but are not often criteria for a major diagnostic labeling. In my practice I have used a computer-based medical record system that permits portrayal and comparison of symptom data to correlate varying degrees of retention of an intramuscular magnesium-loading study (IMMLS) with symptom patterns in 172 patients. The group of patients who show a paradoxical excretion of more Mg than they were given in the IMMLS are a distinctive group with lower blood pressures and significantly fewer digestive and skin symptoms, fewer symptoms of inflammation but more emotional symptoms than those with normal Mg excretion. The group who retained > 49% of the load had higher blood pressures and significantly fewer symptoms of inflammation of the skin and of the reproductive tract.
    Magnesium and trace elements 01/1992; 10(2-4):251-62.
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    ABSTRACT: Numerous studies indicate that alcohol can cause neural and vascular damage in the brain. Additional studies indicate that magnesium ions (Mg2+) possess the ability to modify vascular tone. We utilized an image-splitting television microscope recording system in an intact rat brain model in order to determine whether local (topical) application or systemic (intravenous or intra-arterial) administrations of MgSO4 exert vasodilator effects on cerebral arterioles (66-124 microns o.d.) and venules (66-137 microns o.d.). In addition, we investigated whether infusion of low doses of MgSO4 could modify cerebral vascular spasms induced by ethanol and a calcium mimic, i.e., Ba2+. Topical applications of MgSO4 (i.e., 1-100 mumol) in male and female rats produced dose-dependent dilations of cerebral arterioles and venules; male animals were clearly more sensitive to Mg2+. Systemic infusion of low doses of MgSO4 (i.e., 1.0 and 4.0 mumol/min) into the femoral vein or a branch of the internal carotid artery failed, completely, to induce changes in arterial blood pressure or diameter of arterioles and venules. However, such nonvasodilator doses of MgSO4, infused via either route, inhibited contractile responses induced by 5% Ba2+ and 10% ethanol in arterioles and venules in a dose-dependent manner in both male and female rats. Cerebral microvessels of male animals were more sensitive to inhibitory actions of Mg2+ against Ba(2+)-induced microvascular constrictions than were microvessels of females. Administration of a variety of pharmacologic antagonists as well as a cyclo-oxygenase inhibitor failed to influence either the local vasodilator effects of Mg2+ or the inhibitory actions of Mg2+. Basal plasma levels of Mg were higher in female vs. male rats (1.98 +/- 0.06 vs. 1.77 +/- 0.028 mg/dl). Systemic administration of MgSO4 in cerebral nonvasodilator doses resulted in rapid elevation of plasma Mg levels in a dose-dependent manner (e.g., 0.3-4.3 mg/dl over control levels). Plasma Mg levels were more elevated in female than male animals. It is concluded that magnesium ions can act as local vasodilators, in physiologic doses, on brain microvessels and that these divalent cations possess antispasmodic activities, in nonvasodilator doses, on intact rat brain arterioles and venules. In addition, our findings suggest that Mg2+ might be useful in the treatment and prevention of alcohol-induced brain vascular damage.
    Magnesium and trace elements 01/1992; 10(2-4):269-80.
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    ABSTRACT: The availability of methods to assess intracellular magnesium has caused great interest in the biologic role of this ion. Measurement of total intracellular erythrocyte magnesium (RBC Mg) by atomic absorption spectroscopy in 94 prospectively studied patients (87 female, age 44 +/- 12 years) with symptomatic primary mitral valve prolapse diagnosed by strict echocardiographic and clinical criteria (Perloff) identified 35 patients with normal (2.12 +/- 0.16 mmol/l) and 59 with low (1.51 +/- 0.31 mmol/l) RBC Mg (mean +/- SD). The two groups did not differ in demographic or clinical characteristics, incidence of thick mitral leaflets, joint hypermobility (by Beighton-Horan score), chest pain, fatigability, palpitations, anxiety, depression, orthostatic hypotension, autonomic test results or plasma catecholamines. Muscle cramps and migraines were more frequent in Mg-deficient patients (but p < 0.05). We postulate that the lack of differences between the groups may be due to poor correlation of RBC Mg with Mg concentration of tissue pools.
    Magnesium and trace elements 01/1992; 10(2-4):205-14.

  • Magnesium and trace elements 01/1992; 10:182-192.
  • R Vink ·
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    ABSTRACT: Nuclear magnetic resonance (NMR) studies of central nervous system (CNS) trauma have shown that intracellular free magnesium (Mg) concentration declines following injury. This fall in free Mg concentration was associated with a decrease in brain total tissue Mg concentration. Declines in both free and total tissue Mg concentration could be prevented or attenuated by treatments targeted to improve neurologic outcome by inhibition of specific injury factors, such as excitatory amino acids and opioid peptides. Furthermore, the extent of these changes in CNS Mg concentration and their attenuation with a diversity of treatments have been correlated to neurologic outcome. As such, it has been proposed that Mg, and in particular the cytosolic free Mg concentration, plays a critical central role in determining the degree of neurologic deficit expressed following a traumatic injury to the CNS. This mini-review will focus on the evidence suggesting that Mg concentration is important in the development of irreversible tissue damage following traumatic brain injury, and will discuss the relative importance of Mg to this process, and its interrelationship with a number of other proposed injury factors.
    Magnesium and trace elements 01/1991; 10(1):1-10.
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    ABSTRACT: A novel ion selective electrode (ISE) for ionized magnesium (IMg2+) in whole blood (WB), plasma (PL), and serum (S) has been designed. We have undertaken a number of studies, experimental and clinical, to characterize and examine the linearity, precision, specificity, accuracy, and utility of this new ISE for IMg2+ in WB, S, and PL of normal human subjects, diseased subjects and animals. Using aqueous solutions, mean IMg2+ values are within 94.6-99.2% of their targets. The linearity of the ISE (0.1-3.0 mM) in aqueous solutions, and human PL and S ranges between 92.0 and 99.3%. The ISE is highly selective for IMg2+, yielding measurements in less than 2 min, and exhibiting no or negligible effects from pathophysiologic concentrations of Ca2+, Na+, K+, H+ or NH4+. Likewise such concentrations of heavy metals (e.g., Fe3+, Cu2+, Zn2+, Cd2+, Hg2+ and Pb2+) in aqueous solution and serum do not interfere with ISE measurements for IMg2+. Ligand binding studies in aqueous solution indicate that pathophysiologic concentrations of different anions (e.g., heparin, bicarbonate, phosphate, acetate, sulfate and lactate) bind to Mg2+ with varying intensities, effectively reducing its concentration in solutions. IMg2+ measurements on WB, PL, and S for a given person's samples are virtually identical. Typically, IMg2+ is 71% of total Mg (TMg) but varies from subject to subject. The IMg2+ is held within a narrow range (0.53-0.67 mM) in normal, healthy controls. Studies on diseased human subjects (i.e., cardiac cases, cardiopulmonary bypass, abnormal pregnancy, renal transplant recipients, diabetics, asthmatics, etc.) indicate that IMg2+ levels often exhibit significant alterations from normality, despite no change in TMg.(ABSTRACT TRUNCATED AT 250 WORDS)
    Magnesium and trace elements 01/1991; 10(2-4):90-8.
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    ABSTRACT: In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.
    Magnesium and trace elements 01/1991; 10(2-4):122-35.
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    ABSTRACT: A study was undertaken to learn whether the young Mg-deficient mammal can respond to major stress with increased levels of plasma corticosterone. Plasma corticosterone was determined in 48 weanling rats with dietary Mg deficiency and in 48 Mg-sufficient controls fed a Mg-supplemented diet, studying 12 animals at a time on experimental day 14. Each animal was studied once, either in an unstressed state or after the stress of audiogenic or strychnine seizures. Plasma corticosterone was determined using a radioimmunoassay; Mg was analyzed by atomic absorption spectrophotometry. On experimental day 14, unstressed Mg-deficient rats were tremulous, hyperirritable and showed slightly increased plasma corticosterone levels that exceeded controls levels. After strychnine shock, the mean plasma corticosterone levels of Mg-sufficient and Mg-deficient rats were both significantly increased over resting levels, and were not statistically different. Moreover, the spontaneous mortality rate that occurred during the experimental period in all Mg-sufficient rats was 0 compared to 27% among all Mg-deficient animals (p less than 0.0001). It was concluded that young rats deficient in Mg for 2 weeks could respond to major stress with levels of plasma corticosterone that were not significantly different from values of equally stressed Mg-sufficient controls. The deficient animals suffered a higher mortality, providing support for the concept that Mg deficiency increases stress-induced mortality in animals.
    Magnesium and trace elements 01/1991; 10(1):40-6.
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    ABSTRACT: The antiarrhythmic actions of high [Mg]o (8 mM) were studied in sheep cardiac Purkinje fibers. At 0.1 microM, strophanthidin inhibits the Na-K pump (intracellular sodium activity aiNa and force increase) and increasing Mg shortens the action potential, decreases force and increases aiNa, as in control. At 1 microM, strophanthidin increases aiNa and force, induces oscillatory potentials (Vos) and arrhythmias: increasing Mg reduces Vos and abolishes arrhythmias but increases aiNa further. High Mg also slows or stops spontaneous activity induced by norepinephrine by a positive shift of the threshold, and decreases Vos in high [Ca]o. Thus, antiarrhythmic mechanisms of high [Mg]o include a shift in threshold potential and a decrease in Vos but not a removal of Na pump inhibition.
    Magnesium and trace elements 01/1991; 10(5-6):355-63.
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    ABSTRACT: 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.
    Magnesium and trace elements 01/1991; 10(5-6):409-19.