Magnesium
It appears that proper levels of magnesium are
important as a preventive of heart disease
Scientific Studies on Magnesium
Other Pages Within
the Karl Loren Webs:
The Great Magnesium Scare Hoax - Guess Who Profited?
How Important is Magnesium When Taking Calcium?
How Potasium and Magnesium Work Together
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Record 1 from database: MEDLINE
- Title
- Disorders of magnesium metabolism.
- Author
- Nadler JL; Rude RK
- Address
- Department of Diabetes, Endocrinology and Metabolism, City of Hope Medical Center,
Duarte, California, USA.
- Source
- Endocrinol Metab Clin North Am, 1995 Sep, 24:3, 623-41
- Abstract
- Magnesium depletion is more common than previously thought. It seems to be especially
prevalent in patients with diabetes mellitus. It is usually caused by losses from the
kidney or gastrointestinal tract. A patient with magnesium depletion may present with
neuromuscular symptoms, hypokalemia, hypocalcemia, or cardiovascular complication.
Physicians should maintain a high index of suspicion for magnesium depletion in patients
at high risk and should implement therapy early.
- Language of Publication
- English
- Unique Identifier
- 96106640
- MeSH Heading (Major)
- Magnesium|*ME/PH; Magnesium Deficiency|*/CO/EP/ET/PP
- MeSH Heading
- Bone and Bones|ME/PH; Cardiovascular Physiology; Cardiovascular System|ME/PH;
Homeostasis|PH; Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0889-8529
- Country of Publication
- UNITED STATES
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Record 2 from database: MEDLINE
- Title
- Should we supplement magnesium in critically ill patients?
- Author
- Olerich MA; Rude RK
- Address
- Department of Diabetes, Los Angeles County/University of Southern California Medical
Center 90033.
- Source
- New Horiz, 1994 May, 2:2, 186-92
- Abstract
- Magnesium (Mg) deficiency is a common yet underdiagnosed problem in the ICU. Since only
1% of total body Mg is in the extracellular fluid, serum Mg concentrations may not
adequately reflect Mg status. Utilizing techniques to measure intracellular Mg
concentrations, Mg depletion has been shown to be present in about one half of all ICU
patients. These patients have significantly higher morbidity and mortality rates than
Mg-replete patients. Accurate identification of patients with Mg depletion requires a
knowledge of the risk factors associated with Mg deficiency. These factors include poorly
controlled diabetes mellitus, alcohol ingestion, severe diarrhea and steatorrhea, and the
use of a number of pharmacologic agents that induce renal Mg wasting. Manifestations of Mg
deficiency include hypokalemia, hypocalcemia, neuromuscular hyperexcitability, respiratory
muscle weakness, and intractable arrhythmias. Mg deficiency may also play a role in the
genesis of myocardial ischemia. In this article, we review the assessment, causes, and
manifestations of Mg deficiency and suggest guidelines for adequate treatment.
- Language of Publication
- English
- Unique Identifier
- 95006764
- MeSH Heading (Major)
- Magnesium|*TU; Magnesium Deficiency|BL/CO/DI/*DT/EP
- MeSH Heading
- Clinical Protocols; Critical Illness; Drug Monitoring; Human; Infusions, Intravenous;
Injections, Intravenous; Intensive Care Units; Nutrition Assessment; Parenteral Nutrition,
Total|MT; Risk Factors; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Survival
Rate
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1063-7389
- Country of Publication
- UNITED STATES
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Record 3 from database: MEDLINE
- Title
- Magnesium homeostasis and clinical disorders of magnesium deficiency.
- Author
- Whang R; Hampton EM; Whang DD
- Address
- Veterans Affairs (VA) Medical and Regional Office Center, Honolulu, HI.
- Source
- Ann Pharmacother, 1994 Feb, 28:2, 220-6
- Abstract
- OBJECTIVE: To survey the causes of clinical hypomagnesemia and Mg deficiency. The
relationship of hypomagnesemia to digitalis toxicity, congestive heart failure,
arrhythmias, and acute myocardial infarction is discussed, as is the clinical
interrelationship of Mg and K concentrations, the principal intracellular cations. DATA
SOURCES: A MEDLINE search and retrieval was used to identify relevant references. STUDY
SELECTION: Clinical reports, as well as studies, were selected for this review. DATA
EXTRACTION: There were very few placebo-controlled clinical studies. Clinical observations
were related primarily to compilation of series in which Mg was administered and clinical
results reported. In addition, conclusions derived from review articles on the subject of
clinical Mg depletion were used. DATA SYNTHESIS: Clinical diagnosis of Mg deficiency is
ascertained most expeditiously by estimating serum Mg concentrations. Although available
on order by physicians, the lack of routine serum Mg analysis as part of the
"electrolyte panel" impedes the diagnosis of clinical Mg deficiency. Renal loss
of Mg resulting from the widespread use of loop diuretics is responsible for significant
numbers of patients with Mg deficiency and hypomagnesemia. Life-threatening cardiac
arrhythmias and seizures represent the most serious manifestations of clinical
hypomagnesemia and Mg depletion. In the most critically ill patients, treatment with
intravenous Mg is recommended. Oral repletion of Mg is reserved for the less critically
ill hospitalized patients and ambulatory patients. Close attention must be paid to
optimizing K replenishment in hypokalemic patients by concurrent treatment of any
accompanying hypomagnesemia to avoid the problem of refractory K repletion. CONCLUSIONS:
Hypomagnesemia is one of the most frequent serum electrolyte abnormalities in current
clinical practice. Routine inclusion of serum Mg analysis in the electrolyte panel will
enhance the clinical recognition and treatment of hypomagnesemic Mg-depleted patients.
Failure to respond to treatment of recurrent ventricular tachycardia/fibrillation to usual
antiarrhythmic therapy in patients with acute myocardial infarction, idiopathic dilated
cardiomyopathy, and congestive heart failure should alert the clinician to consider
administering intravenous Mg. Repair of coexisting hypomagnesemia in hypokalemic patients
is essential to avoid the problem of refractory K repletion caused by coexisting Mg
depletion. More controlled clinical studies of Mg deficiency are necessary to ascertain
the cost-effectiveness of Mg replacement therapy.
- Language of Publication
- English
- Unique Identifier
- 94227310
- MeSH Heading (Major)
- Magnesium|BL/*ME/TU; Magnesium Deficiency|*/CO/ET
- MeSH Heading
- Arrhythmia|ET; Heart Failure, Congestive|CO; Homeostasis; Human; Hypertension|CO;
Hypokalemia|CO
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1060-0280
- Country of Publication
- UNITED STATES
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Record 4 from database: MEDLINE
- Title
- Should magnesium therapy be considered for the treatment of coronary heart disease? I. A
critical appraisal of current facts and hypotheses.
- Author
- Weiss M; Lasserre B
- Address
- Department of Internal Medicine, Anna Seiler Haus, Inselspital, Berne, Switzerland.
- Source
- Magnes Res, 1994 Jun, 7:2, 135-44
- Abstract
- When given at physiological doses, therapy with magnesium corrects the alterations in
cellular function resulting from magnesium deficiency, whereas at higher dosages, which
induce hypermagnesaemic levels, magnesium possesses pharmacological effects, such as the
inhibition of the calcium influx: this may alter the electrophysiological properties of
heart cells, decrease catecholamine secretion, influence the synthesis of prostacyclin
and/or alter platelet function. The evidence that magnesium deficiency has untoward
effects in patients with ischaemic heart disease is only circumstantial and direct proof
that magnesium deficiency causes cardiac disorders is at present lacking. A ubiquitous
calcium-channel blockade mechanism is the main and well-established way of action whereby
magnesium acts at pharmacological levels; other mechanisms may be involved as well but at
present remain questionable or unsettled. On the basis of the present knowledge,
beneficial effects may thus be expected from high dose intravenous magnesium therapy in
the setting of acute myocardial infarction with respect to mortality rates, even when
there is concurrent thrombolytic therapy, as recently demonstrated by the large LIMIT-2
study, although this could not be confirmed from the ISIS-4 trial. High dose intravenous
magnesium is also a first choice therapy for terminating torsade de pointes ventricular
tachycardia but cannot be considered an established therapy for other cardiac rhythm
disturbances nor for settings other than acute myocardial infarction in the case of
ischaemic heart disease. The preliminary evidence that magnesium deficiency has a high
prevalence in patients with ischaemic heart disease and that it may have a detrimental
influence on the course of ischaemic heart disease needs to be validated by larger
prospective and controlled clinical studies. Magnesium therapy in ischaemic heart disease
thus proves a promising approach which, however, requires that the respective
pharmacological and physiological effects be distinguished and further delineated and that
the type and stage of ischaemic heart disease be characterized.
- Language of Publication
- English
- Unique Identifier
- 95092505
- MeSH Heading (Major)
- Coronary Disease|*DT; Magnesium|PD/*TU; Magnesium Deficiency|CO/EP/*PP
- MeSH Heading
- Animal; Heart|DE/PH; Heart Diseases|CO; Human; Myocardial Infarction|DT; Myocardial
Ischemia|CO; Prevalence
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0953-1424
- Country of Publication
- ENGLAND
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Record 5 from database: MEDLINE
- Title
- A review of magnesium, acute myocardial infarction and arrhythmia.
- Author
- Orlov MV; Brodsky MA; Douban S
- Address
- University of California, Irvine Medical Center, Orange.
- Source
- J Am Coll Nutr, 1994 Apr, 13:2, 127-32
- Abstract
- Many years ago, experimental medicine accumulated substantial evidence that magnesium
(Mg) balance was important for a stable cardiovascular system. Recent clinical interest
was aroused by evidence of decreased mortality in patients with acute myocardial
infarction (AMI), treated with Mg infusions. Pharmacologic actions of Mg include its
antiarrhythmic, antivasospastic and other important cardiovascular effects, substantiating
the rationale for its use in AMI. Direct pharmacologic effect of this ion, rather than
compensation of hypomagnesemia frequently encountered during acute ischemic injury, has
been suggested to account for the above benefits. Several trials studied the efficacy of
early Mg therapy in decreasing mortality from AMI while most of the data point to improved
survival, a few trials could not demonstrate any benefit of Mg. The reported rate of
complications with this therapy is low though the potential for serious side effects
exists. Larger studies of Mg in AMI are expected to resolve the existing controversy.
- Language of Publication
- English
- Unique Identifier
- 94275015
- MeSH Heading (Major)
- Arrhythmia|*DT; Magnesium|AD/AE/PD/PH/*TU; Myocardial Infarction|*DT
- MeSH Heading
- Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0731-5724
- Country of Publication
- UNITED STATES
Record 6 from database: MEDLINE
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- Title
- Magnesium: homeostasis, imbalances, and therapeutic uses.
- Author
- Toto KH; Yucha CB
- Address
-
- Source
- Crit Care Nurs Clin North Am, 1994 Dec, 6:4, 767-83
- Abstract
- Magnesium plays a critical role in numerous metabolic functions, including all reactions
involving adenosine triphosphate, and is thus essential for the production and use of
energy. Magnesium imbalances are common in hospitalized patients, with magnesium
deficiency occurring in 20% to 65% of critically ill patients. This article details the
homeostatic mechanisms regulating magnesium, the functions of magnesium, and the causes,
manifestations, and treatment of both hyper- and hypomagnesemia. Indications and
guidelines for the therapeutic uses of magnesium are also reviewed.
- Language of Publication
- English
- Unique Identifier
- 95283754
- MeSH Heading (Major)
- Magnesium Deficiency|*/DI/ET/TH
- MeSH Heading
- Homeostasis; Human; Magnesium|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0899-5885
- Country of Publication
- UNITED STATES
Return To Top
Record 7 from database: MEDLINE
Title
- Consequences of magnesium deficiency on the enhancement of stress reactions; preventive
and therapeutic implications (a review).
- Author
- Seelig MS
- Address
- Department of Nutrition, School of Public Health, University of North Carolina, Chapel
Hill.
- Source
- J Am Coll Nutr, 1994 Oct, 13:5, 429-46
- Abstract
- Stress intensifies release of catecholamines and corticosteroids that increase survival
of normal animals when their lives are threatened. When magnesium (Mg) deficiency exists,
stress paradoxically increases risk of cardiovascular damage including hypertension,
cerebrovascular and coronary constriction and occlusion, arrhythmias and sudden cardiac
death (SCD). In affluent societies, severe dietary Mg deficiency is uncommon, but dietary
imbalances such as high intakes of fat and/or calcium (Ca) can intensify Mg inadequacy,
especially under conditions of stress. Adrenergic stimulation of lipolysis can intensify
its deficiency by complexing Mg with liberated fatty acids (FA), A low Mg/Ca ratio
increases release of catecholamines, which lowers tissue (i.e. myocardial) Mg levels. It
also favors excess release or formation of factors (derived both from FA metabolism and
the endothelium), that are vasoconstrictive and platelet aggregating; a high Ca/Mg ratio
also directly favors blood coagulation, which is also favored by excess fat and its
mobilization during adrenergic lipolysis. Auto-oxidation of catecholamines yields free
radicals, which explains the enhancement of the protective effect of Mg by anti-oxidant
nutrients against cardiac damage caused by beta-catecholamines. Thus, stress, whether
physical (i.e. exertion, heat, cold, trauma--accidental or surgical, burns), or emotional
(i.e. pain, anxiety, excitement or depression) and dyspnea as in asthma increases need for
Mg. Genetic differences in Mg utilization may account for differences in vulnerability to
Mg deficiency and differences in body responses to stress.
- Language of Publication
- English
- Unique Identifier
- 95138371
- MeSH Heading (Major)
- Magnesium Deficiency|*CO/PC/PP/TH; Stress|*CO/PP
- MeSH Heading
- Adrenal Cortex Hormones|PH; Animal; Cardiovascular System|PP; Catecholamines|PH;
Exertion; Female; Human; Magnesium|AD; Pregnancy
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0731-5724
- Country of Publication
- UNITED STATES
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Record 8 from database: MEDLINE
- Title
- Magnesium and potassium deficiency. Its diagnosis, occurrence and treatment in diuretic
therapy and its consequences for growth, protein synthesis and growth factors.
- Author
- D‡rup I
- Address
- Institute of Physiology, University of Aarhus, Denmark.
- Source
- Acta Physiol Scand Suppl, 1994, 618:, 1-55
- Abstract
- Thiazides and loop diuretics facilitate the loss of K and Mg through the kidneys leading
to deficiencies that may require treatment with supplements. These losses may be
overlooked, however, because serum concentrations may remain normal even when the muscle
concentrations are appreciably reduced. In 76 patients who had received diuretics for 1-17
years, the mean concentrations of K, Mg and Na,K-pumps in skeletal muscle biopsies were
significantly lower than in those from an age- and sexmatched control group, and muscle Mg
and K concentrations were significantly correlated. The serum concentrations, however,
were only below the control range in a few patients. The fact that Mg,K deficiencies may
often be overlooked emphasises the need for data on the contents of skeletal muscle. A
recently developed simple biopsy needle procedure permitted the detection of disorders of
electrolytes during long-term diuretic treatment despite normal serum concentrations. With
the same technique it was possible to detect repletion of the muscle electrolytes after a
Mg supplementation period. Oral Mg supplementation could reestablish normal Mg as well as
K status in patients in long-term diuretic therapy, provided that the supplementation was
maintained for 6 months. Moreover, the normalization of muscle Mg and K was accompanied by
a restoration of the concentration of Na,K-pumps measured as the [3H]ouabain binding site
capacity in skeletal muscle. Mg and K contents were closely correlated in human muscle
biopsies from patients on diuretic treatment, but also in rat muscle which had been
moderately Mg depleted in vivo or in vitro. In isolated soleus muscle, which had been
moderately Mg-depleted in vitro, reduction in cellular K could not be ascribed to reduced
Na,K-pump mediated K-influx. The reduced K content might rather be related to increased K
efflux from the muscles. In rats, insufficient dietary supplies of K, Mg and Zn were
characterized by inhibition of growth and protein synthesis. These effects could not
readily be related to the loss of these elements from muscle tissue, but rather should be
seen as a response to a general deficiency. The most marked evidence of deficiency was
seen in the serum levels, which pointed to the serum concentration as a possible mediator
for the regulation of tissue growth. IGF-I is a low molecular weight peptide possessing
growth promoting properties in many tissues probably as an interplay of both
autocrine/paracrine and endocrine actions. In both animals and man insufficient supplies
of energy and protein are accompanied by growth retardation and a decrease in serum
IGF-I.(ABSTRACT TRUNCATED AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 94310918
- MeSH Heading (Major)
- Magnesium Deficiency|*/CI/DI/TH; Potassium Deficiency|*/CI/DI/TH
- MeSH Heading
- Animal; Diagnosis; Diuretics|AE/TU; Growth Substances|ME; Hormones|ME; Human;
Insulin-Like Growth Factor I|ME; Muscles|ME; Nutrition; Proteins|BI; Support, Non-U.S.
Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0302-2994
- Country of Publication
- ENGLAND
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Record 9 from database: MEDLINE
- Title
- A review of evidence for a role of magnesium and possibly copper deficiency in
necrotizing enterocolitis.
- Author
- Caddell JL
- Address
- Thomas Jefferson University Department of Pediatrics, Philadelphia, PA 19107-6799, USA.
- Source
- Magnes Res, 1996 Mar, 9:1, 55-66
- Abstract
- Necrotizing enterocolitis (NEC) is a neonatal disorder of unknown cause characterized by
rapid necrosis of the bowel, primarily the ileum and colon. It is a worldwide problem. NEC
is the most common gastrointestinal emergency in the neonatal intensive care unit, and
ranks second as a cause of neonatal death. The incidence of NEC is inversely proportional
to the birth weight and the degree of maturity. Infants born at or before 28 weeks
gestational age have not received 80 per cent of the magnesium and 67 per cent of the
copper found at term. Congenital deficiencies of these essential minerals may be
compounded by high renal or gastrointestinal losses and high metabolic demand during the
preterm infant's accelerated growth. Platelet thrombi appear early in the intestinal
microvasculature in NEC. Platelet thrombosis and release of vasoconstrictor, platelet
aggregating thromboxane A2 (TXA2) in human NEC appears to potentiate the intestinal
ischaemia and necrosis in neonates who develop NEC. Magnesium and copper deficiency each
enhance the synthesis of TXA2. Plasma levels of the inflammatory cytokines tumour necrosis
factor (TNF) and interleukin-6 (IL-6) are increased in NEC and in magnesium deficiency;
these experimentally produce shock and tissue injury, especially of the intestine. The
synthesis of the potent vasoconstrictor endothelin is increased in magnesium deficiency.
NEC has been regarded as a luminal insult that causes local generation of destructive
oxygen free radicals. Tissues from animals deficient in magnesium are more susceptible to
oxidative injury and lipid peroxidation than tissues from normal animals. Magnesium and
copper deficiency impair antioxidant defence through decreased synthesis of glutathione
and reduced activity of Cu/Zn superoxide dismutase, respectively. Although the aetiology
of NEC is unknown, there appears to be sufficient data to implicate magnesium and possibly
copper deficiencies in the pathogenesis. Consequences of deficiency of one or both
minerals may include increased synthesis or activity of injurious mediators: IL-1, IL-6,
TNF, TXA2, endothelin, and oxygen free radicals. A prospective trial of magnesium
supplementation, but not copper supplementation, in very premature neonates can be
recommended, with NEC as one of the outcome measures.
- Language of Publication
- English
- Unique Identifier
- 96416189
- MeSH Heading (Major)
- Copper|BL/*DF; Enterocolitis, Pseudomembranous|EP/*ET/PP; Infant, Premature,
Diseases|EP/*ET/PP; Intestines|*PP; Magnesium Deficiency|*/BL/CO/PP
- MeSH Heading
- Free Radicals; Human; Incidence; Infant, Newborn; Reactive Oxygen Species|PH; Support,
Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0953-1424
- Country of Publication
- ENGLAND
Return To Top
Record 10 from database: MEDLINE
- Title
- Significance of magnesium in congestive heart failure.
- Author
- Douban S; Brodsky MA; Whang DD; Whang R
- Address
- Department of Medicine, University of California, Irvine Medical Center, Orange
92668-3298, USA.
- Source
- Am Heart J, 1996 Sep, 132:3, 664-71
- Abstract
- Electrolyte balance has been regarded as a factor important to cardiovascular stability,
particularly in congestive heart failure. Among the common electrolytes, the significance
of magnesium has been debated because of difficulty in accurate measurement and other
associated factors, including other electrolyte abnormalities. The serum magnesium level
represents < 1% of total body stores and does not reflect total-body magnesium
concentration, a clinical situation very similar to that of serum potassium. Magnesium is
important as a cofactor in several enzymatic reactions contributing to stable
cardiovascular hemodynamics and electrophysiologic functioning. Its deficiency is common
and can be associated with risk factors and complications of heart failure. Typical
therapy for heart failure (digoxin, diuretic agents, and ACE inhibitors) are influenced by
or associated with significant alteration in magnesium balance. Magnesium therapy, both
for deficiency replacement and in higher pharmacologic doses, has been beneficial in
improving hemodynamics and in treating arrhythmias. Magnesium toxicity rarely occurs
except in patients with renal dysfunction. In conclusion, the intricate role of magnesium
on a biochemical and cellular level in cardiac cells is crucial in maintaining stable
cardiovascular hemodynamics and electrophysiologic function. In patients with congestive
heart failure, the presence of adequate total-body magnesium stores serve as an important
prognostic indicator because of an amelioration of arrhythmias, digitalis toxicity, and
hemodynamic abnormalities.
- Language of Publication
- English
- Unique Identifier
- 96393253
- MeSH Heading (Major)
- Heart Failure, Congestive|DT/ET/*PP; Magnesium|AN/BL/*PH/TU
- MeSH Heading
- Arrhythmia|DT; Electrophysiology; Hemodynamics; Human; Magnesium Deficiency|CO/PP;
Potassium|BL; Prognosis; Risk Factors; Tissue Distribution; Water-Electrolyte Balance
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-8703
- Country of Publication
- UNITED STATES
Return To Top
Record 11 from database: MEDLINE
- Title
- New concepts in the cardioprotective action of magnesium and taurine during the calcium
paradox and ischaemia of the heart.
- Author
- Suleiman MS
- Address
- Department of Physiology, University of Bristol, UK.
- Source
- Magnes Res, 1994 Dec, 7:3-4, 295-312
- Abstract
- A rise in intracellular sodium during periods of exposure to calcium free media would
seem to be the critical step that predisposes the mammalian heart to the damaging effects
of the calcium paradox. The damage which is seen in both single cells and multicellular
preparations, occurs on reperfusion with calcium containing media and results from calcium
loading via the sodium/calcium exchanger where the rise in intracellular calcium provokes
hypercontraction as well as activating hydrolytic enzymes. Because the rise in
intracellular sodium is a critical step in inducing damage, manoeuvres which reduce this
rise during calcium depletion are expected to protect the heart against the calcium
paradox. Raising extracellular magnesium concentration is one such manoeuvre which by
blocking the influx of sodium through the L-type calcium channels, reduces the rise in
intracellular sodium during calcium depletion. The beta-amino acid taurine is another
agent capable of opposing a rise in intracellular sodium. Taurine is present at high
concentration in mammalian heart cells and is maintained against high concentration
gradient. During calcium depletion, heart cells use this energy to efflux taurine and
sodium via a taurine/sodium symport and therefore protect against the calcium paradox. A
similar mechanism may also be used by the ischaemic heart to reduce the rise in
intracellular sodium. In contrast to the changes seen during the calcium paradox the
ischaemic heart shows a rise in intracellular magnesium concentration. This rise will have
several and diverse cellular effects including the modulation of intracellular calcium
mobilisation and of several membrane transporters. The potential significance of these
effects remains to be evaluated. On the other hand elevated levels of extracellular
magnesium may protect the ischaemic heart by reducing the influx of calcium by suppressing
the L-type calcium channels and possibly the sodium/calcium exchanger. Finally evidence
suggests that the rat heart may not be identical to that of other species in its response
to the calcium paradox and to the protective role of intracellular taurine and
extracellular magnesium. The reason for this species difference would seem to be due to
different metabolic activity and the activity of the sodium, potassium-ATPase.
- Language of Publication
- English
- Unique Identifier
- 95306268
- MeSH Heading (Major)
- Calcium|*AE/ME; Magnesium|ME/*PD/TU; Myocardial Ischemia|ME/*PP; Myocardial Reperfusion
Injury|ME/*PP; Taurine|*PD/TU
- MeSH Heading
- Animal; Calcium Channels|DE/ME; Carrier Proteins|ME; Guinea Pigs; Human; Intracellular
Fluid|ME; Muscle Proteins|ME; Rabbits; Rats; Sodium|ME; Species Specificity
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0953-1424
- Country of Publication
- ENGLAND
Return To Top
Record 12 from database: MEDLINE
- Title
- Magnesium and its therapeutic uses: a review.
- Author
- McLean RM
- Address
- Department of Medicine, Yale School of Medicine, New Haven, Connecticut 06510.
- Source
- Am J Med, 1994 Jan, 96:1, 63-76
- Abstract
- Magnesium has been reported as an effective medical therapy in an expanding array of
conditions. Evidence investigating magnesium's use is presented, with a number of studies
suggesting it should be seriously considered in such conditions as ischemic heart disease,
cardiac arrhythmias, and asthma. Magnesium balance and metabolism are briefly reviewed,
and then various hypotheses are presented that may explain magnesium's physiologic
mechanisms of action, most likely involving calcium and potassium flux across cellular
membranes in smooth muscle. In a number of the conditions to be discussed, it has been
uncertain whether magnesium administration serves the purpose of merely correcting an
underlying deficiency state or of utilizing a specific pharmacologic effect of magnesium.
Magnesium deficiency is a relatively common condition, and predisposing factors as well as
recent methods for assessing total body stores of magnesium are discussed. Physicians
should be familiar with the numerous conditions and therapeutics that are risk factors for
an underlying magnesium deficiency and in which empiric magnesium replacement should be
considered. Guidelines for administration of parenteral magnesium are presented with
specific focus on the low risk of adverse effects, as suggested by the large and rapid
dosing regimens used in many of the clinical studies discussed here.
- Language of Publication
- English
- Unique Identifier
- 94136508
- MeSH Heading (Major)
- Magnesium|ME/PD/*TU
- MeSH Heading
- Alcoholism|DT; Arrhythmia|DT; Asthma|DT; Calcium|ME; Female; Human; Magnesium
Deficiency|ME; Myocardial Ischemia|DT; Potassium|ME; Pre-Eclampsia|DT; Pregnancy;
Substance Withdrawal Syndrome|DT
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
-
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There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life.
Check out our companion site, at: http://www.oralchelation.net
where Karl's 2000 page book is published. Karl Loren is the author and
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for another web site about ORAL CHELATION.
His personal philosophical articles are at PHILOSOPHY.
Copyright © May 20, 2008 6:24 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED.
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