Inflammation, arterial

Several chemical compounds may cause inflammation or constriction of the blood vessel wall (vasoconstriction). Ergot alkaloids at high doses cause constriction and thickening of the vessel wall. Allylamine may also induce constriction of coronary arteries, thickening of their smooth muscle walls, and a disease state that corresponds to coronary heart disease. The culprit is a toxic reactive metabolite of allylamine, acrolein, that binds covalently to nucleophilic groups of proteins and nucleic acids in the cardiac myocytes. 

Salicylic acid reduces inflammation, including inflammation of the arteries. In arteries it can work to prevent hardening and narrowing. 

With regard to epinephrines potential adverse cardiac effects, it is important to remember that in anaphylaxis, the heart is a target organ. Mast cells located between myocardial fibers, in perivascular tissue, and in the arterial intima are activated through IgE and other mechanisms to release chemical mediators of inflammation, including histamine, leukotriene C4, and prostaglandin D2. Coronary artery spasm, myocardial injury, and cardiac dysrhythmias have been documented in some patients before epinephrine has been injected for treatment of anaphylaxis, as well as in patients with anaphylaxis who have not been treated with epinephrine [11, 12]. 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

Although atherosclerosis and rheumatoid arthritis (RA) are distinct disease states, both disorders are chronic inflammatory conditions and may have common mechanisms of disease perpetuation. At sites of inflammation, such as the arterial intima undergoing atherogen-esis or the rheumatoid joint, oxygen radicals, in the presence of transition-metal ions, may initiate the peroxidation of low-density lipoprotein (LDL) to produce oxidatively modified LDL (ox-LDL). Ox-LDL has several pro-inflammatory properties and may contribute to the formation of arterial lesions (Steinberg et /., 1989). Increased levels of lipid peroxidation products have been detected in inflammatory synovial fluid (Rowley et /., 1984 Winyard et al., 1987a Merry et al., 1991 Selley et al., 1992 detailed below), but the potential pro-inflammatory role of ox-LDL in the rheumatoid joint has not been considered. We hypothesize that the oxidation of LDL within the inflamed rheumatoid joint plays a pro-inflammatory role just as ox-LDL has the identical capacity within the arterial intima in atherosclerosis. 

Ebselen is a seleno-oiganic that mimics glutathione peroxidase and inhibits iron-stimulated lipid peroxidation. It significandy reduced both inferct size and oedema progression in the middle cerebral artery exclusion (MCAO) focal model of stroke in tats (Matsui et al. 1990). Ebselen has also been shown to be an effective anti-inflammatory agent in a H202-dependent inflammation model in tats (Parnham 1991). 

Endothelial dysfunction, inflammation, and the formation of fatty streaks contribute to the formation of atherosclerotic coronary artery plaques, the underlying cause of coronary artery disease (CAD). The predominant cause of ACS, in more than 90% of patients, is atheromatous plaque rupture, Assuring, or erosion of an unstable atherosclerotic plaque that occludes less than 50% of the coronary lumen prior to the event, rather than a more stable 70% to 90% stenosis of the coronary artery.3 Stable stenoses are characteristic of stable angina. 

Atherosclerosis A disease process of the arteries involving fatty plaque formation and inflammation in the vascular wall. 

Hozawa, A, Jacobs, DR, Jr., Steffes, MW, Gross, MD, Steffen, LM, and Lee, DH, 2007. Relationships of circulating carotenoid concentrations with several markers of inflammation, oxidative stress, and endothelial dysfunction The Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) study. Clin Chem 53,447 455. 

If persistent, these molecules (coding for inflammation, oxidative stress, remodeling, and thrombosis) can cause endothelial dysfunction and acceleration of arthrosclero-sis progression [117]. SWNTs were shown also to alter the cardiac activity by affecting the arterial baroreflex function (BRF) of sinus mode in rats exposed by intratracheal instillation [118]. 

Bobryshev YV, Cherian SM, Inder SJ, Lord RSA (1999) Neovascular expression of VE-cadherin in human atherosclerotic arteries in its relation to intimal inflammation. Cardiovasc Res 43 1003-1017... 

Zanger D, Yang BK, Ardans J, Waclawiw MA, Csako G, Wahl LM, Cannon RO III (2000) Divergent effects of hormone therapy on serum markers of inflammation in postmenopausal women with coronary artery disease on appropriate medical management. J Am Coll Cardiol 36 1797-1802... 

Arterial thrombosis. The formation of an aggregate of blood factors (thrombus), primarily platelets and fibrin, with entrapment of cellular elements in the arteries. Arthritis. Inflammation of a joint. 

Widlansky, M.E., Duffy, S.J., Hamburg, N.M., Gokce, N., Warden, B.A., Wiseman, S., Keaney, J.F., Jr., Frei, B., and Vita, J.A., Effects of black tea consumption on plasma catechins and markers of oxidative stress and inflammation in patients with coronary artery disease. Free Radical Biol Med, 38, 499, 2005. 

In the summer of 1840 Robert Mayer, while performing a simple operation of bloodletting on board a Dutch ship in Java, was so startled by the bright red color of the venous blood that he feared for a moment that he might have opened an artery by mistake (283). Although he was unaware of Adair Crawford s experiments on the influence of temperature on the color of venous blood in living animals, which were published in the Experiments and Observations on Animal Heat and the Inflammation of Combustible Bodies in 1788, Mayer reasoned that in a hot climate, such as that of Java, the human body needed less internal combustion in order to maintain its temperature. Two years later he formulated the law of the equivalence between heat and work (283). 

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