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10.1097/MAJ.0b013e3181aaee4d http://scihub22266oqcxt.onion/10.1097/MAJ.0b013e3181aaee4d C3753099!3753099!19593099     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Med+Sci 2009 ; 338 (1): 22-7 Nephropedia Template TP {{tp|p=19593099|t=2009. Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia |pdf=|usr=}}{{19593099}} gab.com Text Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia JO: Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=19593099 #FOAvip Hypomagnesemia continues to be a significant clinical disorder that is present in patients with diabetes mellitus, alcoholism, and treatment with magnesuric drugs (diuretics, cancer chemotherapy agents, etc.). To determine the role of magnesium in cardiovascular pathophysiology, we have used dietary restriction of this cation in animal models. This review has highlighted some key observations which helped formulate the hypothesis that release of substance P (SP) during experimental dietary Mg deficiency (MgD) may initiate a cascade of deleterious inflammatory, oxidative, and nitrosative events, which ultimately promote cardiomyopathy, in situ cardiac dysfunction, and myocardial intolerance to secondary stresses. SP acts primarily through neurokinin-1 (NK-1) receptors of inflammatory and endothelial cells, and may: induce production of reactive oxygen and nitrogen species (superoxide anion, NO?, peroxynitrite, hydroxyl radical), leading to enhanced consumption of tissue antioxidants; stimulate release of inflammatory mediators; promote tissue adhesion molecule expression; and enhance inflammatory cell tissue infiltration and cardiovascular lesion formation. These SP-mediated events may predispose the heart to injury if faced with subsequent oxidative stressors (ischemia/reperfusion, certain drugs) or facilitate development of in situ cardiac dysfunction, especially with prolonged dietary Mg-restriction. Significant protection against most of these MgD-mediated events has been observed with interventions that modulate neuronal SP release or its bioactivity, and with several antioxidants (vitamin E, probucol, epicaptopril, d-propranolol). In view of the clinical prevalence of hypomagnesemia, new treatments, beyond magnesium repletion, may be needed to diminish deleterious neurogenic and prooxidative components described in this article. Twit Text FOAVip Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia ????Am J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=19593099 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19593099 #FOAvip English Wikipedia <ref>{{Cite pmid|19593099}}</ref> Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia #MMPMID19593099 Kramer JH; Spurney C; Iantorno M; Tziros C; Mak IT; Tejero-Taldo MI; Chmielinska JJ; Komarov AM; Weglicki WB Am J Med Sci 2009[Jul]; 338 (1): 22-7 PMID19593099show ga Hypomagnesemia continues to be a significant clinical disorder that is present in patients with diabetes mellitus, alcoholism, and treatment with magnesuric drugs (diuretics, cancer chemotherapy agents, etc.). To determine the role of magnesium in cardiovascular pathophysiology, we have used dietary restriction of this cation in animal models. This review has highlighted some key observations which helped formulate the hypothesis that release of substance P (SP) during experimental dietary Mg deficiency (MgD) may initiate a cascade of deleterious inflammatory, oxidative, and nitrosative events, which ultimately promote cardiomyopathy, in situ cardiac dysfunction, and myocardial intolerance to secondary stresses. SP acts primarily through neurokinin-1 (NK-1) receptors of inflammatory and endothelial cells, and may: induce production of reactive oxygen and nitrogen species (superoxide anion, NO?, peroxynitrite, hydroxyl radical), leading to enhanced consumption of tissue antioxidants; stimulate release of inflammatory mediators; promote tissue adhesion molecule expression; and enhance inflammatory cell tissue infiltration and cardiovascular lesion formation. These SP-mediated events may predispose the heart to injury if faced with subsequent oxidative stressors (ischemia/reperfusion, certain drugs) or facilitate development of in situ cardiac dysfunction, especially with prolonged dietary Mg-restriction. Significant protection against most of these MgD-mediated events has been observed with interventions that modulate neuronal SP release or its bioactivity, and with several antioxidants (vitamin E, probucol, epicaptopril, d-propranolol). In view of the clinical prevalence of hypomagnesemia, new treatments, beyond magnesium repletion, may be needed to diminish deleterious neurogenic and prooxidative components described in this article. äNeurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia (epmc).pdf DeepDyve Pubget Overpricing