In this study, we have examined the effects of variation in dietary Mg on the atherogenic process. Oral supplementation of rabbits fed a high cholesterol diet (1% or 2%) with the Mg salt magnesium aspartate hydrochloride (Magnesiocard) (i) lowers the level of serum cholesterol and triglycerides in normal (25-35%) as well as atherosclerotic (20-40%) animals and (ii) attenuates the atherosclerotic process markedly. In addition, we found that dietary deficiency of Mg augments atherogenesis markedly and stimulates (or activates) macrophages of the reticuloendothelial system. Evidence is presented to indicate that the hypercholesterolemic state may cause the loss of Mg from soft tissues to the serum, thereby masking an underlying Mg deficiency.Hypercholesterolemia has been widely accepted as a high risk factor for development of atherosclerosis and ischemic heart disease (IHD) (1-3), particularly since cholesterol-rich diets lead to deposition of lipids in blood vessel walls and an atherosclerotic-like state in experimental animals (4-6). Increased blood levels of lipoproteins are thought to eventually lead to endothelial cell injury or denudation with concomitant uptake of the former molecules (7,8), increased permeability to calcium ions (Ca2") (9), invasion of the arterial wall by macrophages (10-12), and altered smooth muscle cells (7,8,13). It is, however, not clear how the lipoproteins and Ca2+ gain access to the normally and relatively impermeable arterial walls (4-13).Approximately 20 years ago, it was suggested on the basis of epidemiologic findings that the incidence of IHD was highest in geographic regions with soft drinking water (14). Of the minerals that are deficient in soft water, magnesium (Mg) is the only element that has been found to be consistently lowered in cardiac muscle of IHD victims (for reviews, see refs. 15 and 16 (15,16,20,28).Recent emphasis on the potential importance of nutritional factors and preventive rather than palliative medicine in the approach to etiology and treatment of cardiovascular disease led us to examine the effects of a possible "hidden" Mg deficiency as well as the potential benefits of Mg supplementation on the development of atherosclerosis induced by high cholesterol diets in rabbits. We report here that dietary deficiency of Mg (compatible with the reduced dietary intake of Mg seen in the adult population of the Western World; see refs. 29-31), which often is not reflected by serum analysis, exacerbates atherogenesis and stimulates (or activates) macrophages of the reticuloendothelial system (RES). In addition, we demonstrate that pretreatment of animals with orally administered magnesium aspartate hydrochloride (Magnesiocard) (i) attenuates the atherosclerotic process markedly and (ii) lowers serum cholesterol and triglycerides in normal as well as in some atherosclerotic animals. Finally, evidence is presented to indicate that a high serum cholesterol seems to obscure the Mg deficiency that is present in the atherosclerotic animal. METHODS Animals and ...
Excised gastrocnemii from 2–4-month-old normal and genetically dystrophic mice (Jackson Memorial Laboratory strains) were studied at 15°C which permits prolonged uniform maintenance of standard responses. Results are averages from muscles of generally 10–14 diseased or normal animals. Normal muscles (87 mg) produce maximal twitch and tetanus tensions of respectively 23.9 and 53.1 gm; dystrophic muscles (35 mg) correspondingly yield 3.3 and 14.6 gm. Thus, compared to normal, dystrophic muscles are atrophied, weaker (directly or in tension output/gm muscle), and show a smaller twitch/tetanus tension ratio. The contraction period time is the same for both muscle types (about 59 msec.), but the dystrophic relaxation period is 3 times longer (676 as against 224 msec.). The dystrophic active state duration (to end of plateau) is shorter than the normal (9.8 as against 14.4 msec.). At rest, both muscle types possess nonlinear elasticity, but the diseased are stiffer.
Excised gastrocnemii of normal and dystrophic mice, directly stimulated in long series of isometric twitches or tetani, show different fatigue patterns. During a series of 1,200 maximal twitches, developed tension drops much more slowly in dystrophic responses so that final output relative to initial is: dystrophic, 70%, normal, 10%. A similar but smaller difference holds for a tetanus series. Pronounced quantitative and qualitative distinctions between the two muscle types also appear in the changes of other twitch characteristics: relaxation time and rate, and contraction rate but not time. The qualitatively distinct fatigue pattern of the dystrophic muscle is dependent not on diffusional differences stemming from its smaller bulk, but on some basic dissimilarity inherent in the dystrophic myopathy. The possible nature of this dissimilarity is discussed in relation to general functional features of fatigue and to special aspects of dystrophic muscle concerned with metabolism, intensity property of the active state, and role of the relaxing factor.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.