1. Human aortocoronary grafts and nitric oxide release: relationship to pulsatile pressure 
Thomas V Bilfinger, MD, George B Stefano, PhD 
The Annals of Thoracic Surgery 
Volume 69, Issue 2, Pages (February 2000)
DOI: /S (99)

2. Fig 1 Experimental design.
The Annals of Thoracic Surgery  , DOI: ( /S (99) )

3. Fig 2
NO determinations during pulsatile pressure at 30 cycles per minute with peak pressures of 110 and 170 mm Hg. Both the internal thoracic artery (A) and the saphenous vein (B) released NO in response to transient pressure changes. Arrows indicate p less than 0.05 when comparing the two pressures from four mean replicate values per vessel. In the vein, the decreased NO peak values, after 32 minutes of high-pressure pulsation, were significantly decreased further, as noted by the arrows (p < 0.05).
The Annals of Thoracic Surgery  , DOI: ( /S (99) )

4. Fig 3
Exposure of blood vessels for 1 hour to constant pressure followed by morphine (10−6 M) exposure. Both the internal thoracic artery (A) and saphenous vein (B), at different pressures, responded differently to the same dose of morphine. A significant increase of NO following the initial morphine exposure (arrows) regardless of the pressure was observed.
The Annals of Thoracic Surgery  , DOI: ( /S (99) )

5. Fig 4
The response of internal thoracic artery and saphenous vein to increasing concentrations of morphine at different pressures.
The Annals of Thoracic Surgery  , DOI: ( /S (99) )

6. Fig 5
Granulocyte adhesion to internal thoracic artery or saphenous vein endothelial surface after 1 hour of constant exposure of the vessels to different pressures. (∗p < 0.05 for treatments 1 through 3 compared to each other; ∗∗p < 0.05 in treatment 4 where artery values are compared to vein, indicating a lack of morphine effect on granulocyte adherence.)
The Annals of Thoracic Surgery  , DOI: ( /S (99) )