Suppression of smooth muscle cell proliferation after experimental PTFE arterial grafting: A role for polyclonal anti-basic fibroblast growth factor (bFGF) antibody

B. Randone, A. Cucina, P. Graziano, V. Corvino, G. Cavallaro, I. Palmieri, A. Cavallaro, A. V. Sterpetti

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)401-407
Number of pages7
JournalEuropean Journal of Vascular and Endovascular Surgery
Volume16
Issue number5
Publication statusPublished - 1998

Fingerprint

Fibroblast Growth Factor 2
Smooth Muscle Myocytes
Cell Proliferation
Antibodies
Inbred Lew Rats
Transplants
Abdominal Aorta
Intraperitoneal Injections
Thoracic Aorta
Ambulatory Surgical Procedures
Postoperative Period
Inhalation
Hyperplasia
Anesthetics
Weights and Measures
Control Groups

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Radiology Nuclear Medicine and imaging
  • Surgery

Cite this

Suppression of smooth muscle cell proliferation after experimental PTFE arterial grafting : A role for polyclonal anti-basic fibroblast growth factor (bFGF) antibody. / Randone, B.; Cucina, A.; Graziano, P.; Corvino, V.; Cavallaro, G.; Palmieri, I.; Cavallaro, A.; Sterpetti, A. V.

In: European Journal of Vascular and Endovascular Surgery, Vol. 16, No. 5, 1998, p. 401-407.

Research output: Contribution to journalArticle

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title = "Suppression of smooth muscle cell proliferation after experimental PTFE arterial grafting: A role for polyclonal anti-basic fibroblast growth factor (bFGF) antibody",
abstract = "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.",
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AU - Randone, B.

AU - Cucina, A.

AU - Graziano, P.

AU - Corvino, V.

AU - Cavallaro, G.

AU - Palmieri, I.

AU - Cavallaro, A.

AU - Sterpetti, A. V.

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N2 - 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.

AB - 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.

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