1. Volume 5, Issue 3, Pages 167-184 (December 1998)
The role of leukocyte-endothelial cell adhesion in cardiovascular disease 
Michael J. Eppihimer 
Pathophysiology 
Volume 5, Issue 3, Pages (December 1998)
DOI: /S (98)

2. Fig. 1
Mechanism proposed to explain the accumulation of leukocytes in myocardial tissue exposed to ischemia and reperfusion. Elevation in ROMs, inflammatory mediators and complement activation induces an elevation in leukocyte and endothelial cell adhesion molecules, and consequently, an increase in leukocyte adhesion and emigration and tissue injury.
Pathophysiology 1998 5, DOI: ( /S (98) )

3. Fig. 2
Mechanism proposed to explain the accumulation of leukocytes in cerebral tissue exposed to ischemia and reperfusion. Elevation in ROMs, which is potentiated by NO, and inflammatory mediators induces an elevation in leukocyte and endothelial cell adhesion molecules, and consequently, an increase in leukocyte adhesion and emigration and tissue injury.
Pathophysiology 1998 5, DOI: ( /S (98) )

4. Fig. 3
Mechanism proposed to explain the accumulation of leukocytes in atherosclerotic lesions. Elevation in ox-LDLs produces a concomitant reduction in NO. This is paralleled by an increase in ROMs and other inflammatory mediators. A subsequent increase in leukocyte and endothelial cell adhesion molecules leads to an increase in leukocyte adhesion and emigration. The release of inflammatory mediators from emigrated leukocytes produces a chemotactic signal, which amplifies the magnitude of leukocyte adhesion and emigration. The differentiation of monocytes into macrophages, and their uptake of cholesterol produces the formation of foam cells. In addition to foam cells, growth factors released by emigrated leukocytes induce cell proliferation and consequently, the development of an atherosclerotic lesion.
Pathophysiology 1998 5, DOI: ( /S (98) )