Page 249 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

C. Response to Injury Hypothesis of Atherosclerosis Genesis
Smoking Diabetes mellitus Hyperhomo- Age
cysteinemia
Hypertension
Lumen Genetic risk factors
Hyperlipidemia (LDL)
Male
Endothelium 1
Intima
Chlamydia infection ?
Endothelial damage
Media
2 3
Lipid permeability Monocyte adhesion Thrombocyte aggregation
and immigration Atherosclerosis II
Monocyte
Macrophage

LDL
4
Transformation in Plate 7.33
macrophages
Chemotactic and
growth factors
Release of
O 2 radicals
Immigration and
– proliferation of
NO O 2 myocytes in the intima
–
NO+O 2 → ONOO – 6
5
Proliferation
Lack of NO action
LDL oxidation
8 Myocytes
Vasodilation
7
Oxidized LDL
Spasm
Changed
receptor behavior

9
LDL phagocytosis
10
Scavenger
receptor
Foam cell Foam cell
Plaque (atheroma)
239

Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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