Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart

Eiichi Watanabe, D. M. Smith, J. Sun, F. W. Smart, J. B. Delcarpio, T. B. Roberts, C. H. Van Meter, W. C. Claycomb

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Abstract

Administration of growth factors is emerging as a new therapeutic approach for the enhancement of collateral vessel formation in the ischemic heart. We have investigated the effects of intramyocardial delivery of FGF-2 in the presence and absence of heparin on angiogenesis in a porcine model of myocardial infarction. Yorkshire pigs were subjected to myocardial infarction by the placement of an embolization coil in the left anterior descending artery (n = 5). Four to five weeks after creation of an infarct, FGF-2 (10 μg) alone or in complex with heparin, heparan sulfate, or heparin agarose beads was injected either into the normal myocardium or along the infarct border area. Histologic evaluation of each injection site was performed 4 to 5 weeks post-injection. The effect of FGF-2 on angiogenesis was evaluated by determining the number of capillaries (diameter < 20 μm( and arterioles (> 20 μm with tunica media) in each area observed. The number of capillaries were not affected by the treatment of FGF-2 both in normal myocardium and infarct border area. However, in the normal myocardium, the number of arterioles were increased with the treatment of FGF-2 alone (85 ± 59%, P < 0.04), FGF-2 plus heparin (281 ± 193%, P < 0.004) and FGF-2-coated heparin beads (241 ± 141%, P < 0.01), as compared to control. Delivery of FGF-2 into the infarct border area, also increased the number of arterioles when FGF-2 was given with heparin (736 ± 154%, P < 0.001) or heparin heads (700 ± 109%, P < 0.001), as compared to control. FGF-2 administered with heparin was the most effective method of enhancing angiogenesis as compared to FGF-2 alone, FGF-2 plus heparan sulfate, or FGF-2 coated heparin agarose beads.

Original languageEnglish
Pages (from-to)30-37
Number of pages8
JournalBasic Research in Cardiology
Volume93
Issue number1
DOIs
Publication statusPublished - 01-02-1998

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Fibroblast Growth Factor 2
Swine
Heparin
Myocardium
Heparitin Sulfate
Arterioles
Myocardial Infarction
Tunica Media
Injections
Intercellular Signaling Peptides and Proteins
Therapeutics
Arteries

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Watanabe, E., Smith, D. M., Sun, J., Smart, F. W., Delcarpio, J. B., Roberts, T. B., ... Claycomb, W. C. (1998). Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart. Basic Research in Cardiology, 93(1), 30-37. https://doi.org/10.1007/s003950050059
Watanabe, Eiichi ; Smith, D. M. ; Sun, J. ; Smart, F. W. ; Delcarpio, J. B. ; Roberts, T. B. ; Van Meter, C. H. ; Claycomb, W. C. / Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart. In: Basic Research in Cardiology. 1998 ; Vol. 93, No. 1. pp. 30-37.
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Watanabe, E, Smith, DM, Sun, J, Smart, FW, Delcarpio, JB, Roberts, TB, Van Meter, CH & Claycomb, WC 1998, 'Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart', Basic Research in Cardiology, vol. 93, no. 1, pp. 30-37. https://doi.org/10.1007/s003950050059

Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart. / Watanabe, Eiichi; Smith, D. M.; Sun, J.; Smart, F. W.; Delcarpio, J. B.; Roberts, T. B.; Van Meter, C. H.; Claycomb, W. C.

In: Basic Research in Cardiology, Vol. 93, No. 1, 01.02.1998, p. 30-37.

Research output: Contribution to journalArticle

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T1 - Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart

AU - Watanabe, Eiichi

AU - Smith, D. M.

AU - Sun, J.

AU - Smart, F. W.

AU - Delcarpio, J. B.

AU - Roberts, T. B.

AU - Van Meter, C. H.

AU - Claycomb, W. C.

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N2 - Administration of growth factors is emerging as a new therapeutic approach for the enhancement of collateral vessel formation in the ischemic heart. We have investigated the effects of intramyocardial delivery of FGF-2 in the presence and absence of heparin on angiogenesis in a porcine model of myocardial infarction. Yorkshire pigs were subjected to myocardial infarction by the placement of an embolization coil in the left anterior descending artery (n = 5). Four to five weeks after creation of an infarct, FGF-2 (10 μg) alone or in complex with heparin, heparan sulfate, or heparin agarose beads was injected either into the normal myocardium or along the infarct border area. Histologic evaluation of each injection site was performed 4 to 5 weeks post-injection. The effect of FGF-2 on angiogenesis was evaluated by determining the number of capillaries (diameter < 20 μm( and arterioles (> 20 μm with tunica media) in each area observed. The number of capillaries were not affected by the treatment of FGF-2 both in normal myocardium and infarct border area. However, in the normal myocardium, the number of arterioles were increased with the treatment of FGF-2 alone (85 ± 59%, P < 0.04), FGF-2 plus heparin (281 ± 193%, P < 0.004) and FGF-2-coated heparin beads (241 ± 141%, P < 0.01), as compared to control. Delivery of FGF-2 into the infarct border area, also increased the number of arterioles when FGF-2 was given with heparin (736 ± 154%, P < 0.001) or heparin heads (700 ± 109%, P < 0.001), as compared to control. FGF-2 administered with heparin was the most effective method of enhancing angiogenesis as compared to FGF-2 alone, FGF-2 plus heparan sulfate, or FGF-2 coated heparin agarose beads.

AB - Administration of growth factors is emerging as a new therapeutic approach for the enhancement of collateral vessel formation in the ischemic heart. We have investigated the effects of intramyocardial delivery of FGF-2 in the presence and absence of heparin on angiogenesis in a porcine model of myocardial infarction. Yorkshire pigs were subjected to myocardial infarction by the placement of an embolization coil in the left anterior descending artery (n = 5). Four to five weeks after creation of an infarct, FGF-2 (10 μg) alone or in complex with heparin, heparan sulfate, or heparin agarose beads was injected either into the normal myocardium or along the infarct border area. Histologic evaluation of each injection site was performed 4 to 5 weeks post-injection. The effect of FGF-2 on angiogenesis was evaluated by determining the number of capillaries (diameter < 20 μm( and arterioles (> 20 μm with tunica media) in each area observed. The number of capillaries were not affected by the treatment of FGF-2 both in normal myocardium and infarct border area. However, in the normal myocardium, the number of arterioles were increased with the treatment of FGF-2 alone (85 ± 59%, P < 0.04), FGF-2 plus heparin (281 ± 193%, P < 0.004) and FGF-2-coated heparin beads (241 ± 141%, P < 0.01), as compared to control. Delivery of FGF-2 into the infarct border area, also increased the number of arterioles when FGF-2 was given with heparin (736 ± 154%, P < 0.001) or heparin heads (700 ± 109%, P < 0.001), as compared to control. FGF-2 administered with heparin was the most effective method of enhancing angiogenesis as compared to FGF-2 alone, FGF-2 plus heparan sulfate, or FGF-2 coated heparin agarose beads.

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