Response to injury theory of atherosclerosis, microcirculation

3 Pages
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Department
Biomedical Science
Course Code
BMS 420
Professor
Charles Miller

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Description
7 September Average pressure Radius Tension Aorta 95 1 cm 140,000 Capillary 25 3 μm 10 Vena cava 10 1.4 cm 18,000 Venules do not have continuous vascular smooth muscle, but they do have some segments Less compliant aorta Higher pulse pressure Less steady flow to capillaries (more intermittent) More work for heart Thicker left ventricle (possible failure) Compliance decreases with age Lower compliance – more pressure generated per unit volume Response to injury theory of atherosclerosis Endothelial cells are first to be injured Possibly permeability changes related to toxins High blood pressure Viruses Smoking Platelets, macrophages stick to wall Vascular smooth muscle cells proliferate and migrate to intima Foam cells appear when VSMC and macrophages take up lipids 75% of cross-sectional area – see symptoms while sitting (passive) 55% - see symptoms while exercising Fatty streak In intima area LDL cholesterol accumulates between the endothelium and connective tissue and is oxidizied Macrophages ingest cholesterol and become foam cells Smooth muscle cells, attracted by macrophage cytokines, begin to divide and take up cholesterol Stable fibrous plaque A
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