1. Tissue factor and thrombin mediate myocardial ischemia-reperfusion injury 
Albert J Chong, MD, Timothy H Pohlman, MD, Craig R Hampton, MD, Akira Shimamoto, MD, PhD, Nigel Mackman, PhD, Edward D Verrier, MD 
The Annals of Thoracic Surgery 
Volume 75, Issue 2, Pages S649-S655 (February 2003)
DOI: /S (02)04691-X

2. Fig 1
Coagulation cascade. Tissue factor (TF) initiates the extrinsic coagulation cascade, leading to generation of thrombin and fibrin. Thrombin induces upregulation of TF expression in monocytes and endothelial cells, resulting in a positive feedback loop. X = coagulation factor X; Xa = activated coagulation factor X; Xase = coagulation factor X activation.
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)

3. Fig 2
Expression of tissue factor (TF). Tissue factor is constitutively expressed at low-levels in monocytes and endothelial cells intravascularly, and in the vascular adventitial layer and cardiomyocytes extravascularly. The endothelium prevents the exposure of subendothelial TF from plasma coagulation factors.
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)

4. Fig 3
Tissue factor mRNA (TF mRNA) expression after myocardial ischemia/reperfusion (I/R) injury. TF mRNA levels were determined by Northern blotting and normalized to levels of glyceraldehyde-3-phosphate dehydrogenase (G3PDH). (A) Determination of TF mRNA levels in two separate samples from non-AR areas (N) of LV of three independent sham-operated rabbits. (B) Comparison of TF mRNA levels in the non-AR areas (N) of LV with levels in the AR areas of LV of three independent I/R-injured rabbits. (Reprinted from [34], with permission.) AR = at-risk; LV = left ventricle.
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)

5. Fig 4
Tissue factor (TF) antigen upregulation in ischemic cardiomyocytes. (A) Regional increase in TF staining of ischemic cardiomyocytes in fixed heart tissue from a rabbit after I/R injury. Tissue factor-positive areas stain dark red. (B) Serial section stained with acid-fuchsin to identify ischemic cardiomyocytes (reddish brown). (C) Tissue factor expression in the AR (at risk) area of LV (left ventricle) of I/R-injured rabbit compared with (D) normal (non-AR area) of same rabbit. (E) Minimal TF expression observed in vascular endothelium (arrowhead) and increased TF expression observed in cardiomyocytes (arrow). Tissue factor–positive cells stain brown. lu = lumen. (F) Serial section stained with control antibody. (G) The sheep antirabbit TF polyclonal antibody was detected with a fluorescein isothiocyanate–labeled antibody and stains green. The mouse anti-CD31 monoclonal antibody was detected with a Texas red–labeled antibody and stains red. (H) Analysis of TF and vWF expression. The anti-TF monoclonal antibody was stained green and the antirabbit vWF antibody was stained red. (Reprinted from [34], with permission.)
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)

6. Fig 5
Ultrastructural analysis of myocardium from I/R-injured rabbits. (A) Normal capillary from the LV (left ventricle) myocardium of a control rabbit. (B) Injured capillary in an AR (at risk) area of myocardium of an I/R-injured rabbit (arrow indicates endothelial disruption). (Reprinted from [34], with permission.)
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)

7. Fig 6
Effect of anti–tissue factor antibody (anti-TF Ab) treatment on infarct size. (A) Rabbits were treated with either saline (n = 5, hatched bars) or an antirabbit TF monoclonal antibody (n = 6, black bars) 15 minutes before ischemia. Similar AR areas of the left ventricle (LV) were observed in both groups (42 2% for antirabbit TF antibody group and 39% 5% for saline-treated rabbits). The infarct size was significantly reduced in the antibody treatment group (16% ± 1% for the antirabbit TF antibody group and 41% ± 1% for the saline-treated rabbits, p = 0.004). (B) Rabbits were treated with saline (n = 5) or antirabbit TF monoclonal antibody (n = 5) 30 minutes after onset of ischemia. Similar AR areas of LV were observed in both groups (47% ± 4% for antirabbit TF antibody group and 44% ± 1% for saline-treated rabbits). The infarct size was significantly reduced in the antibody treatment group (24% ± 4% for the antirabbit TF antibody rabbits and 43% ± 1% for saline-treated group, p = 0.014). Data are expressed as mean ± SE. (Reprinted from [34], with permission.)
The Annals of Thoracic Surgery  , S649-S655DOI: ( /S (02)04691-X)