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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The circulatory effects of norepinephrine (4 micrograms/kg), isoproterenol (10 micrograms/kg) and phenylephrine (20 micrograms/kg) were determined in anesthetized dogs with normal plasma magnesium and with induced hypermagnesemia. Norepinephrine caused a 24% increase in heart rate and a 103% increase in the systemic vascular resistance index in normomagnesemic dogs, while with hypermagnesemia the variations were of 13% and 1%, respectively. Isoproterenol increased heart rate by 48% and 18% in dogs with normo- and hypermagnesemia, respectively. Phenylephrine increased the systemic vascular resistance index (74%) only in the normomagnesemic state. The effects of all the drugs were significantly different (P less than 0.01), without and with the simultaneous administration of magnesium sulfate (plasma magnesium, 1.3 +/- 0.2 mEq/l and 6.8 +/- 1.1 mEq/l, respectively). We conclude that acute induced hypermagnesemia antagonizes the circulatory effects of adrenergic stimulation, a fact that may explain its antiarrhythmic and hemodynamic effects during acute myocardial ischemia.
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PMID:The antiadrenergic effects of hypermagnesemia: an experimental study. 182 14

In-vitro experiments are presented which indicate that the concentration of extracellular magnesium ions ([Mg2+]o) can exert profound influences on the contractility and reactivity of arteries, arterioles and veins from a number of regional vasculatures in several mammalian species, including man. Hypomagnesemia can potentiate the contractile activity of a variety of neurohumoral substances and induce vasospasm. Hypermagnesemia can do the reverse, i.e., induce hyporeactivity, relaxation and vasodilatation. Data are also presented to indicate that [Mg2+]o can control the entry, distribution and exit of calcium ions (Ca2+) from vascular smooth muscle cells. Arterial and venous smooth muscles excised from rats with alloxan-diabetes mellitus or spontaneous hypertension (SHR) appear to exhibit vascular membranes which have modifications in their Mg-Ca exchange sites. Data are reviewed which suggest that certain vascular diseases (e.g., sudden-death ischemic heart disease, hypertension, eclampsia, diabetes mellitus) are associated with a Mg-deficiency. Overall, it is suggested that [Mg2+]o and membrane [Mg] may play critical roles in regulating vascular tone and homeostasis.
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PMID:Hypomagnesemia and vasoconstriction: possible relationship to etiology of sudden death ischemic heart disease and hypertensive vascular diseases. 730 71

Magnesium is an important constituent of the intracellular space that affects a number of intracellular and whole body functions. Magnesium balance depends on intake and renal excretion, which is regulated mainly in the thick ascending limb of the loop of Henle. The complex hormonal modulation that responds to changes in plasma concentration of other ions such as calcium and potassium is lacking for magnesium. As a result, negative magnesium balance results in a prompt decrease in plasma magnesium concentration, and hypermagnesemia accompanies renal failure with magnesium accumulation. Hypomagnesemia may result from gastrointestinal losses or renal losses, the latter due to primary renal magnesium wasting or in association with sodium loss. Hypomagnesemia may arise together with and contribute to the persistence of hypokalemia and hypocalcemia. The major direct toxicity of hypomagnesemia is cardiovascular. When urgent correction of hypomagnesemia is required, as with myocardial ischemia, post cardiopulmonary bypass, and torsades de pointes, intravenous or intramuscular magnesium sulfate should be used. Oral magnesium preparations are available for chronic use.
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PMID:Hypomagnesemia: renal magnesium handling. 945 89

Until recently the physiological role of magnesium was essentially ignored. However, with the development of new technologies to measure the intracellular free concentration of magnesium ([Mg2+]i), the biologically important fraction, there has been an explosion of interest in the molecular, biochemical, physiological and pharmacological functions of magnesium. In addition improved methods for assessing magnesium status in the clinic have contributed to the further understanding of magnesium regulation in health and disease. Magnesium deficiency is now considered to contribute to many diseases and the role for magnesium as a therapeutic agent is being tested in numerous large clinical trials. This review focuses on clinical manifestations associated with magnesium deficiency and highlights the clinical significance of hypermagnesemia. Specific clinical conditions in which magnesium deficiency has been implicated to play a pathophysiological role, namely hypertension, ischemic heart disease, arrhythmias, prec-eclampsia, asthma and critical illness will be discussed and the possible therapeutic role of magnesium will be considered. Although there is still much to be learnt regarding the exact role of magnesium in clinical medicine, there are two conditions where magnesium is now considered the therapeutic agent of choice, pre-eclampsia and torsades de pointes. Future research, both at the fundamental and clinical levels, will certainly facilitate our understanding of how magnesium contributes to pathological processes and under what circumstances it should be used therapeutically.
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PMID:Magnesium in clinical medicine. 1497 44