Arteriosclerosis prevention

In the vasculature, ANG H not only increases contraction of smooth muscle cells, but is also able to induce vascular injury. This can be prevented by blocking NFkB activation [3] suggesting a link between ANG II and inflammation processes involved in the pathogenesis of arteriosclerosis (see below). Thus, ACE inhibitors not only decrease vascular tone but probably also exert vasoprotective effects. 

ACE inhibitors inhibit the degradation of bradykinin and potentiate the effects of bradykinin by about 50-100-fold. The prevention of bradykinin degradation by ACE inhibitors is particularly protective for the heart. Increased bradykinin levels prevent postischemic reperfusion arrhythmia, delays manifestations of cardiac ischemia, prevents platelet aggregation, and probably also reduces the degree of arteriosclerosis and the development of cardiac hypertrophy. The role of bradykinin and bradykinin-induced NO release for the improvement of cardiac functions by converting enzyme inhibitors has been demonstrated convincingly with use of a specific bradykinin receptor antagonist and inhibitors of NO-synthase. 

Mammals lack the ability to synthesize astaxanthin or convert dietary astaxanthin into vitamin A. Unlike p-carotene, astaxanthin has no pro-vitamin activity in these animals. Astaxanthin has been shown in both in vitro and in a study with human subjects to be effective for the prevention of the oxidation of low-density protein, suggesting that it can be used to prevent arteriosclerosis, coronary artery disease, and ischemic brain development. A number of astaxanthin health products are under study. 

Shimizu, K. et al., Host CD40 ligand deficiency induces long-term allograft survival and donor-specific tolerance in mouse cardiac transplantation but does not prevent graft arteriosclerosis, J. Immunol., 165, 3506, 2000. 

Aside from its use as an antimalarial compound, quinine is used for the prevention and treatment of nocturnal leg muscle cramps, especially those resulting from arthritis, diabetes, thrombophlebitis, arteriosclerosis, and varicose veins. 

Schaffer LW, Davidson JT, Vlasuk GP, Dunwiddie CT, Siegel PKS. Selective factor Xa inhibition by recombinant antistasin prevents vascular graft thrombosis in baboons. Arteriosclerosis and Thromb 1992 12 879-885. 

The determination of cholesterol is important for the diagnosis and prevention of a number of clinical disorders such as hypertension, arteriosclerosis, cerebral thrombosis and coronary heart disease. As the majority of cholesterol in human blood is present in an esterified form, a separate saponification step is required to obtain a total cholesterol analysis early methods for this involved caustic and toxic reagents, long analysis times and a relatively large sample volume. Free cholesterol can be determined chromatographically, although this requires cumbersome and expensive laboratory-based equipment. Modern methods use the enzyme cholesterol esterase to release esterified cholesterol which is then oxidised by a second enzyme, cholesterol oxidase (ChOx, Fig. 23.3) [48]. 

Transfection of animals with plasmid DNA encoding murine soluble Flt-1 (sFlt-1) prevents the early vascular inflammation and late arteriosclerosis. Since... 

From 1952 to 1962, several experimental studies using rats fed a choline-deficient diet reported the development of aortic arteriosclerosis.171-173 Using rats fed a choline-deficient diet, Sidransky et al.174 reported that elevated (2%) dietary tryptophan affected the elevated serum lipid levels of rats fed the choline-deficient diet for 1 week. Within 1 week the added dietary tryptophan to the choline-deficient diet caused a return in serum cholesterol, HDL cholesterol, and triglyceride values to levels present in rats fed the choline-supplemented diet. The significance of the alterations in serum lipids due to added dietary tryptophan was unknown, but it stressed that a specific amino acid (L-tryptophan) excess created a further nutritional imbalance, which could influence the altered circulating serum lipids due to choline deficiency. The alterations in serum lipid due to choline deficiency were thought to influence the development of arteriosclerosis in the rat, and possibly the added dietary tryptophan was able to prevent the effect. Further experimental studies are needed to determine whether this speculation was valid. 

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