Regulation of new blood vessel growth into ischemic skeletal muscle

R. L. Bush, William C Pevec, A. Ndoye, A. T W Cheung, J. Sasse, D. N. Pearson

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Purpose: In a rabbit model, transposition of a muscle pedicle flap to an ischemic hind limb has been shown to result in the development of new blood vessels that connect the arterial circulation of the flap to the circulation of the limb. The hypothesis that exogenous recombinant basic fibroblast growth factor (bFGF) would enhance the development of this new blood supply was examined and the regulation of bFGF in this process was investigated. Methods: The right common iliac artery was ligated in 12 male New Zealand white rabbits. An abdominal wall muscle flap based on the left inferior epigastric artery was transposed to the right thigh. bFGF in phosphate- buffered saline (PBS) at 3 ng/h (n = 6), or PBS alone (n = 6), was infused for 7 days via mini-osmotic pumps with an infusion catheter positioned at the flap-muscle interface. The flap-muscle interface was immunostained with anti- α-actin antibody to determine blood vessel density (number of vessels/mm) and with anti-bFGF antibody to evaluate bFGF distribution. RNA was isolated from these sections, and polymerase chain reaction (PCR) was used to examine endogenous bFGF messenger RNA (mRNA) expression. Results: Blood vessel density was significantly increased in animals receiving exogenous bFGF (22.0 ± 10.6 vessels/mm vs. 10.7 ± 8.8 vessels/mm, P = .009). In the controls, neovessels were arranged in clusters with endogenous bFGF concentrated around these clusters. In bFGF-treated animals, vessels were diffusely scattered throughout the flap limb interface, corresponding to the distribution pattern of infused bFGF. There was no difference in bFGF mRNA expression between the control and the bFGF-treated groups. Conclusion: Exogenous bFGF infusion significantly augmented new blood vessel development at the flap-limb interface. Endogenous bFGF was up-regulated around the newly developed microvessels in control animals, and vessel growth correlated with the diffuse distribution of exogenous bFGF, implicating bFGF as an important factor in angiogenesis. Exogenous bFGF did not affect bFGF mRNA expression, suggesting that the regulation of bFGF is not under autocrine control.

Original languageEnglish (US)
Pages (from-to)919-928
Number of pages10
JournalJournal of Vascular Surgery
Volume28
Issue number5
StatePublished - 1998

Fingerprint

Fibroblast Growth Factor 2
Blood Vessels
Skeletal Muscle
Growth
Extremities
Muscles
Messenger RNA
Phosphates
Epigastric Arteries
Rabbits
Abdominal Muscles
Infusion Pumps
Iliac Artery
Angiogenesis Inducing Agents
Abdominal Wall
Thigh
Microvessels

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Bush, R. L., Pevec, W. C., Ndoye, A., Cheung, A. T. W., Sasse, J., & Pearson, D. N. (1998). Regulation of new blood vessel growth into ischemic skeletal muscle. Journal of Vascular Surgery, 28(5), 919-928.

Regulation of new blood vessel growth into ischemic skeletal muscle. / Bush, R. L.; Pevec, William C; Ndoye, A.; Cheung, A. T W; Sasse, J.; Pearson, D. N.

In: Journal of Vascular Surgery, Vol. 28, No. 5, 1998, p. 919-928.

Research output: Contribution to journalArticle

Bush, RL, Pevec, WC, Ndoye, A, Cheung, ATW, Sasse, J & Pearson, DN 1998, 'Regulation of new blood vessel growth into ischemic skeletal muscle', Journal of Vascular Surgery, vol. 28, no. 5, pp. 919-928.
Bush RL, Pevec WC, Ndoye A, Cheung ATW, Sasse J, Pearson DN. Regulation of new blood vessel growth into ischemic skeletal muscle. Journal of Vascular Surgery. 1998;28(5):919-928.
Bush, R. L. ; Pevec, William C ; Ndoye, A. ; Cheung, A. T W ; Sasse, J. ; Pearson, D. N. / Regulation of new blood vessel growth into ischemic skeletal muscle. In: Journal of Vascular Surgery. 1998 ; Vol. 28, No. 5. pp. 919-928.
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abstract = "Purpose: In a rabbit model, transposition of a muscle pedicle flap to an ischemic hind limb has been shown to result in the development of new blood vessels that connect the arterial circulation of the flap to the circulation of the limb. The hypothesis that exogenous recombinant basic fibroblast growth factor (bFGF) would enhance the development of this new blood supply was examined and the regulation of bFGF in this process was investigated. Methods: The right common iliac artery was ligated in 12 male New Zealand white rabbits. An abdominal wall muscle flap based on the left inferior epigastric artery was transposed to the right thigh. bFGF in phosphate- buffered saline (PBS) at 3 ng/h (n = 6), or PBS alone (n = 6), was infused for 7 days via mini-osmotic pumps with an infusion catheter positioned at the flap-muscle interface. The flap-muscle interface was immunostained with anti- α-actin antibody to determine blood vessel density (number of vessels/mm) and with anti-bFGF antibody to evaluate bFGF distribution. RNA was isolated from these sections, and polymerase chain reaction (PCR) was used to examine endogenous bFGF messenger RNA (mRNA) expression. Results: Blood vessel density was significantly increased in animals receiving exogenous bFGF (22.0 ± 10.6 vessels/mm vs. 10.7 ± 8.8 vessels/mm, P = .009). In the controls, neovessels were arranged in clusters with endogenous bFGF concentrated around these clusters. In bFGF-treated animals, vessels were diffusely scattered throughout the flap limb interface, corresponding to the distribution pattern of infused bFGF. There was no difference in bFGF mRNA expression between the control and the bFGF-treated groups. Conclusion: Exogenous bFGF infusion significantly augmented new blood vessel development at the flap-limb interface. Endogenous bFGF was up-regulated around the newly developed microvessels in control animals, and vessel growth correlated with the diffuse distribution of exogenous bFGF, implicating bFGF as an important factor in angiogenesis. Exogenous bFGF did not affect bFGF mRNA expression, suggesting that the regulation of bFGF is not under autocrine control.",
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N2 - Purpose: In a rabbit model, transposition of a muscle pedicle flap to an ischemic hind limb has been shown to result in the development of new blood vessels that connect the arterial circulation of the flap to the circulation of the limb. The hypothesis that exogenous recombinant basic fibroblast growth factor (bFGF) would enhance the development of this new blood supply was examined and the regulation of bFGF in this process was investigated. Methods: The right common iliac artery was ligated in 12 male New Zealand white rabbits. An abdominal wall muscle flap based on the left inferior epigastric artery was transposed to the right thigh. bFGF in phosphate- buffered saline (PBS) at 3 ng/h (n = 6), or PBS alone (n = 6), was infused for 7 days via mini-osmotic pumps with an infusion catheter positioned at the flap-muscle interface. The flap-muscle interface was immunostained with anti- α-actin antibody to determine blood vessel density (number of vessels/mm) and with anti-bFGF antibody to evaluate bFGF distribution. RNA was isolated from these sections, and polymerase chain reaction (PCR) was used to examine endogenous bFGF messenger RNA (mRNA) expression. Results: Blood vessel density was significantly increased in animals receiving exogenous bFGF (22.0 ± 10.6 vessels/mm vs. 10.7 ± 8.8 vessels/mm, P = .009). In the controls, neovessels were arranged in clusters with endogenous bFGF concentrated around these clusters. In bFGF-treated animals, vessels were diffusely scattered throughout the flap limb interface, corresponding to the distribution pattern of infused bFGF. There was no difference in bFGF mRNA expression between the control and the bFGF-treated groups. Conclusion: Exogenous bFGF infusion significantly augmented new blood vessel development at the flap-limb interface. Endogenous bFGF was up-regulated around the newly developed microvessels in control animals, and vessel growth correlated with the diffuse distribution of exogenous bFGF, implicating bFGF as an important factor in angiogenesis. Exogenous bFGF did not affect bFGF mRNA expression, suggesting that the regulation of bFGF is not under autocrine control.

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