Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23300395
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23300395
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Pediatr+Pharmacol+Ther
2003 ; 8
(1
): 40-5
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Magnesium sulfate for severe acute asthma in children
#MMPMID23300395
Kelly HW
J Pediatr Pharmacol Ther
2003[Jan]; 8
(1
): 40-5
PMID23300395
show ga
Magnesium is an abundant intracellular cation that has been used for years in the
treatment of hyper-tension and seizures associated with eclampsia of pregnancy as
well as used as a tocolytic agent.(1) Over sixty years ago, Haury showed that
magnesium sulfate (MgSO(4)) could produce bronchodilation in asthmatics.(2)
However, interest in magnesium sulfate as a potential therapy for acute asthma
surfaced in the late 1980s following a series of studies demonstrating that
magnesium produced dose-dependent bronchodilation. The precise mechanism by which
magnesium produces smooth muscle relaxation is not known, but it is thought to
act by enhancing calcium uptake in the sarcoplasmic reticulum(3) and/or as a
calcium antagonist.(4) In addition, magnesium is a cofactor regulating a number
of enzymatic and cellular activities in the body, including adenyl cyclase and
sodium-potassium ATP-ase, potentially enhancing the effects of ?2-agonists.(5)
Other potential beneficial mechanisms in asthma include inhibition of
acetylcholine release from cholinergic nerves(6) and reduction of histamine
release from mast cells.(7)It is not clear whether magnesium acts as a functional
antagonist to bronchoconstriction like the ?2-agonists and theophylline or a
specific antagonist like anticholinergics and antihistamines. Studies showing
attenuation of the bronchoconstriction from histamine and methacholine would
suggest functional antagonism.(8,9) Some suggest that the response to intravenous
magnesium sulfate is dependent upon achieving serum magnesium concentrations of
4-6 mg/dL (1.6-2.4 mmol/L).(10) These values are similar to those that are
employed to achieve tocolysis (4-8 mg/dL) and about one half those associated
with severe toxicity of respiratory failure, cardiac arrhythmias and death (12-15
mg/ dL).(1) It should be pointed out that studies have not reported lower
magnesium concentrations in asthmatics than controls although one study reported
correlation with bronchial hyperresponsiveness and intracellular magnesium
concentrations in asthmatics. (11-13) Thus, it is unlikely that the
bronchodilator response to magnesium is a result of restoring normal homeostasis
but most likely a function of its direct antagonistic effects on intracellular
calcium activity.
free
free
free
