SUPPRESSION OF SMOOTH MUSCLE CELL PROLIFERATION AFTER EXPERIMENTAL PTFE ARTERIAL GRAFTING: A ROLE FOR POLYCLONAL ANTI-BASIC FIBROBLAST GROWTH FACTOR (bFGF) ANTIBODY

Objectives: to determine the role of polyclonal anti-basic Fibroblast Growth Factor (bFGF) antibody in inhaling the proliferation of smooth muscle cells after experimental polytetrafluorethilene (PTFE) arterial grafting. Materials: in 14 male inbred Lewis rats (weight 250 mg) a 1 cm long segment of PTFE was interposed at the level of abdominal aorta. Animals were randomised to receive polyclonal anti-bFGF antibody (group A: n = seven animals) or aspecific immunoglobulin (group B: n = seven animals). Anti-bFGF antibody or aspecific immunoglublin were given intraperitoneally at the end of operation, and for the first 2 postoperative days. Animals were sacrificed 7 days after surgery, 24 h after intraperitoneal injection of BromodeoxyUridin (BrdU) to label proliferating smooth muscle cells. Results: one animal in each group died in the immediate postoperative period due to anaesthetic problems. All grafts were patent at the time of sacrifice. BrdU labelling index was statistically higher in the control group B animals at the level of the anastomatic regions (proximal anastomosis: group B 7.9% vs. group A 4.1%. Distal anastomosis: group B 5.1% vs. group A 2.6% p = 0.009) and at the level of PTFE graft (group B 3.8% vs. group A 2.6% p = 0.002), while there was no statistical difference between the control thoracic aorta of the two groups. Main conclusions: bFGF plays a major role in the proliferation of smooth muscle cells at the level of the anastomoses after arterial PTFE grafting. Agents able to block the action of bFGF may be useful in inhibiting the formation of myointimal hyperplasia.

OBJECTIVES: To determine the role of polyclonal anti-basic Fibroblast Growth Factor (bFGF) antibody in inhibiting the proliferation of smooth muscle cells after experimental polytetrafluorethilene (PTFE) arterial grafting. MATERIALS: In 14 male inbred Lewis rats (weight 250 mg) a 1 cm long segment of PTFE was interposed at the level of abdominal aorta. Animals were randomised to receive polyclonal anti-bFGF antibody (group A: n = seven animals) or aspecific immunoglobulin (group B: n = seven animals). Anti-bFGF antibody or aspecific immunoglublin were given intraperitoneally at the end of operation, and for the first 2 postoperative days. Animals were sacrificed 7 days after surgery, 24 h after intraperitoneal injection of BromodeoxyUridin (BrdU) to label proliferating smooth muscle cells. RESULTS: One animal in each group died in the immediate postoperative period due to anaesthetic problems. All grafts were patent at the time of sacrifice. BrdU labelling index was statistically higher in the control group B animals at the level of the anastomotic regions (proximal anastomosis: group B 7.9% vs. group A 4.1%. Distal anastomosis: group B 5.1% vs. group A 2.6% p = 0.009) and at the level of PTFE graft (group B 3.8% vs. group A 2.6% p = 0.002), while there was no statistical difference between the control thoracic aorta of the two groups. MAIN CONCLUSIONS: bFGF plays a major role in the proliferation of smooth muscle cells at the level of the anastomoses after arterial PTFE grafting. Agents able to block the action of bFGF may be useful in inhibiting the formation of myointimal hyperplasia.