thx cece. the following came out of discussion on one of the stickies but belongs out in the general ccsvi area i suspect...
and so, looking at collagen/endothelin-1/magnesium/stents...
Structural alterations of the vascular wall in magnesium‐deficient mice. A possible role of gelatinases A (MMP‐2) and B (MMP) (mice)
http://www.jle.com/fr/revues/medecine/i ... icle.phtml
Magnesium ions are known to protect the cardiovascular system by preventing both calcium accumulation and connective damages, whereas magnesium deficiency induces cardiovascular damages [1, 2]. The vascular lesions of magnesium deficiency are characterized in various animal species by a severe degradation of the extra cellular matrix (ECM) of the connective tissue i.e. by edema, hypertrophy and hyperplasia of the intima, by a thinning and a fragmentation of the internal elastica, by edema, necrosis and hyperplasia of the media. These lesions are accompanied by calcification [3-5].
The integrity of the ECM involves a balance between the synthesis and organization of its structural constituents and their degradation by metalloendopeptidases belonging to the matrixin family [7, 8]. The most important of these endopeptidases belong to the matrix metalloproteinase (MMP) family which, to date, comprises at least 26 members. Among them, the gelatinases MMP-2 and MMP-9, are potent in their ability to cleave gelatins, denatured collagens (IV, V, VII, X), elastin, fibronectin, and TNF-α [6]. A recent report has revealed that MMP-2 can also cleave native collagen I [9] and collagen III [10]. However, it seems that the MMP are capable of degrading all the components of the ECM [11]. The activities of these extracellular metalloproteinases are controlled by specific naturally occurring inhibitors (TIMPs) [7, 11].
The
magnesium-deficient diet used for 42 days in Swiss OF1 mice in the present assay,
led as usual to a severe magnesium deficiency, since magnesium plasma levels were 4-fold decreased as compared to controls [16].
These conditions induced severe alterations of the 2 main connective fibers, elastin and collagens, as described previously by others [4, 5, 17].
Effect of magnesium sulfate on plasma endothelin-1 levels in normal and preeclamptic pregnancies.
http://www.ncbi.nlm.nih.gov/pubmed/1471664
We attempted to determine the effects of magnesium sulfate on: (1) endothelin-1 concentration in preeclampsia, preterm labor, and term pregnancy and (2) endothelin-1 release from human umbilical cord endothelial cells.
METHODS:
Plasma samples were prospectively collected from eight women with preeclampsia, six preterm labor patients, and eight term patients undergoing external cephalic version before and 2 hours after magnesium sulfate infusion.
RESULTS:
Magnesium sulfate infusion in preeclampsia lowered endothelin-1 levels compared with preinfusion values (6.6 +/- 3.81 before and 4.75 +/- 2.28 after infusion, p < 0.02).
CONCLUSION:
A significant reduction of endothelin-1 plasma levels after magnesium sulfate therapy is limited to preeclampsia.
In contrast, this lowering effect was not exhibited in women without preeclampsia or in normal endothelial cells.
hmm needs some further digging then..
Magnesium-deficiency elevates circulating levels of inflammatory cytokines and endothelin (rats)
http://www.springerlink.com/content/481162444r825777/
We have developed two rodent models of diet-induced magnesium-deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions,
the magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-α together with
signigicantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with magnesium deficiency.
now if i can only find some good work involving more humans.
also, i ran across this again - i was sure i had already posted this somewhere but it's not coming up quickly, so here it is again and sorry if this is a repeat!:
Drug-Eluting Bioabsorbable Magnesium Stent
http://onlinelibrary.wiley.com/doi/10.1 ... 081.x/full
Current stent technology is based on the use of permanent implants that remain life long in the vessel wall, far beyond the time required for the prosthesis to accomplish its main goals of sealing dissection and preventing wall recoil. With the possibility to implant long vessel segments using antiproliferative drugs to prevent restenosis, the practice of transforming the coronary vessels into stiff tubes with a full metal jacket covering all side branches and being unable to adjust to the long-term wall changes, including wall remodeling with lumen ectasia becomes a serious concern.
In this article, we describe the first biodegradable stent based on a magnesium alloy that allows controlled corrosion with release to the vessel wall and the blood stream of a natural body component such as magnesium with beneficial antithrombotic, antiarrhythmic, and antiproliferative properties. We also discuss the animal experiments and the initial clinical applications in 20 patients with implants below the knee, with final results soon to be released, and the plans for the first coronary study. The results of these last two studies will indicate whether the absence of a permanent implant and the antiproliferative properties shown in animals are sufficient to prevent the restenotic process in humans or whether the prosthesis must be modified by adding the biodegradable coating with conventional antiproliferative drugs.