Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia

Beskriver hvordan magnesium mangel bidrar til økt utskillelse av Substans P i nociceptorer, som gir økt tilbøyelighet for smertetilstander. Den sier at det ikke holder meg bare magnesiumtilskudd, man må kombinere med antioksidanter også fordi magnesium mangel spiser opp antioksidantforsvaret. Den nevner at graden av magnesium mangel er nesten lineær med graden av Substans P aktivitet og antioksidant nedgang.

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.

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.

Animals placed on Mg-restricted diets also displayed progressive cardiovascular lesion formation, heightened cardiac inflammatory cell infiltration,15 decreased levels of endogenous antioxidants (glutathione, vitamin E, ascorbate) 16,17 and higher plasma levels of pro-oxidant metals 18 and lipid peroxidation (LPO) products.19,20 Antioxidant treatment attenuated the severity of both cardiovascular inflammation in vivo21 and postischemic reperfusion injury in vitro,22 suggesting that dietary Mg-deficiency progresses into a pro-oxidant condition.

The gut is rich in neuropeptides 53 and may contribute to the early rise in plasma SP during MgD. During week 1 of MgD, intestinal inflammation was evident and pronounced PMN infiltration occurred by week 3, when significant decreases in mucosal barrier function were observed.

Varying dietary Mg-intake in rats directly influenced plasma SP levels,58 the associated severity of systemic oxidative/nitrosative stress,59,60 and loss of myocardial tolerance to I/R stress. 58 We demonstrated that SP release also occurred in rats fed moderate MgD diets (MgD20 =20 % RDA; MgD40 = 40% RDA) 58 and the literature suggests that many of the same pathological characteristics observed in the severe MgD9 animal also occurred in these animals. 59,60

Moreover, the decline in RBC glutathione was also directly proportional to the extent of Mg-restriction: levels from MgD40, MgD20, and MgD9 rats fell 20.6%, 29.4%, and 50% compared to the Mg100 group.



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