Atherosclerosis - 1
Atherosclerosis
Michael Oliveira
BS-104-A&P II-MW1
12/01/2012
According to the National Heart Lung and Blood Institute, Atherosclerosis is a disease in which plaque builds up mainly inside the medium to large elastic and muscular arteries that carry oxygenated blood to the heart and other areas of the body. Over time, plaque, made up of fat, cholesterol, calcium, and other substances, hardens and narrows the arteries limiting the flow of oxygen to organs and other parts of the body. This condition is the most significant underlying cause of heart failure, coronary artery disease, strokes and infarction resulting from ischaemia of the heart, brain or extremities.
Atherosclerosis is a matter of the immune and vascular systems. Nitrogen Oxide release protects against atherogenesis by preventing smooth muscle cell proliferation and leukocyte adhesion. When a balance exists in the arteries between nitrogen oxide, a vasodilator, and endothelin-1, a vasoconstrictor, the endothelium is shielded from injury, inflammation, and thrombosis, leukocytes are unable to bind to endothelium, and platelet aggregation is minimized. Excessive NO release, however, may damage vascular wall cells especially in combination with other reactive oxygen intermediates (Matthys & Bult, 1997).
When risk factors for atherosclerosis set in, this balance is disturbed and the immune system fails to counteract or destroy modified LDL, free radicals, infectious and other harmful agents detected by the system as foreign. Monocytes and t-lymphocytes fail to remove or destroy these foreign molecules resulting in the trigger of further immune response, which causes the artery to become inflamed (Boamponsem & Boemponsem, 1997).
Initiation
The regulatory mechanisms of low-density lipoprotein (LDL) receptors function in such a way that the expression of these receptors by a cell is halted when it has taken up enough cholesterol for its metabolic needs. However, lipoprotein particles
Michael Oliveira
BS-104-A&P II-MW1
12/01/2012
According to the National Heart Lung and Blood Institute, Atherosclerosis is a disease in which plaque builds up mainly inside the medium to large elastic and muscular arteries that carry oxygenated blood to the heart and other areas of the body. Over time, plaque, made up of fat, cholesterol, calcium, and other substances, hardens and narrows the arteries limiting the flow of oxygen to organs and other parts of the body. This condition is the most significant underlying cause of heart failure, coronary artery disease, strokes and infarction resulting from ischaemia of the heart, brain or extremities.
Atherosclerosis is a matter of the immune and vascular systems. Nitrogen Oxide release protects against atherogenesis by preventing smooth muscle cell proliferation and leukocyte adhesion. When a balance exists in the arteries between nitrogen oxide, a vasodilator, and endothelin-1, a vasoconstrictor, the endothelium is shielded from injury, inflammation, and thrombosis, leukocytes are unable to bind to endothelium, and platelet aggregation is minimized. Excessive NO release, however, may damage vascular wall cells especially in combination with other reactive oxygen intermediates (Matthys & Bult, 1997).
When risk factors for atherosclerosis set in, this balance is disturbed and the immune system fails to counteract or destroy modified LDL, free radicals, infectious and other harmful agents detected by the system as foreign. Monocytes and t-lymphocytes fail to remove or destroy these foreign molecules resulting in the trigger of further immune response, which causes the artery to become inflamed (Boamponsem & Boemponsem, 1997).
Initiation
The regulatory mechanisms of low-density lipoprotein (LDL) receptors function in such a way that the expression of these receptors by a cell is halted when it has taken up enough cholesterol for its metabolic needs. However, lipoprotein particles
References: Atherosclerosis. (n.d.). Retrieved from http://www.umm.edu/altmed/articles/atherosclerosis-000016.htm Boamponsem A, Boamponsem L. The Role of Inflammation in Atherosclerosis. Advances In Applied Science Research [serial online]. August 2011;2(4):194-207. Available from: Academic Search Complete, Ipswich, MA. Accessed October 31, 2012. Charo I, Taub R. Anti-inflammatory therapeutics for the treatment of atherosclerosis. Nature Reviews Drug Discovery [serial online]. May 2011;10(5):365-376. Available from: Academic Search Complete, Ipswich, MA. Accessed October 31, 2012. Hardening of the arteries. In (2012). D. Dugdale III & D. Zieve (Eds.), A.D.A.M Medical Encyclopedia. A.D.A.M., Inc. Retrieved from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/ Matthys, K. E., & Bult, H. (1997). Nitric oxide function in atherosclerosis. Mediators of Inflammation, 6(1), 3-21. doi: PMC2365845 What Is Atherosclerosis? (2011, July 01). Retrieved from http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis/