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EXPERIMENTAL STUDY

Transendocardial delivery of autologous bone marrow enhances collateral perfusion and regional function in pigs with chronic experimental myocardial ischemia

Shmuel Fuchs, MD^*, Richard Baffour, PhD^*, Yi Fu Zhou, MD^*, Matie Shou, MD^*, Anthony Pierre, BSc^*, Fermin O. Tio, MD, Neil J. Weissman, MD^*, Martin B. Leon, MD, Stephen E. Epstein, MD^* and Ran Kornowski, MD^*

^* the Cardiovascular Research Institute, Washington, DC, USA
Biomedical Research Foundation of South Texas Inc., San-Antonio, Texas, USA
Cardiovascular Research Foundation, Lenox Hill Hospital, New York, New York, USA

Manuscript received December 12, 2000; revised manuscript received January 9, 2001, accepted January 24, 2001.

Reprint requests and correspondence: Dr. Shmuel Fuchs, Cardiovascular Research Institute, Washington Hospital Center, 110 Irving St. Northwest, 4B-1, Washington, DC 20010
sxf6{at}mhg.edu

OBJECTIVES

We tested the hypothesis that intramyocardial injection of autologous bone marrow (ABM) promotes collateral development in ischemic porcine myocardium. We also defined, in vitro, whether bone marrow (BM) cells secrete vascular endothelial growth factor (VEGF) and macrophage chemoattractant protein-1 (MCP-1).

BACKGROUND

The natural processes leading to collateral development are extremely complex, requiring multiple growth factors interacting in concert and in sequence. Because optimal angiogenesis may, therefore, require multiple angiogenic factors, we thought that injection of BM, which contains cells that secrete numerous angiogenic factors, might provide optimal therapeutic angiogenesis.

METHODS

Bone marrow was cultured four weeks in vitro. Conditioned medium was assayed for VEGF and MCP-1 and was added to cultured pig aortic endothelial cells (PAEC) to assess proliferation. Four weeks after left circumflex ameroid implantation, freshly aspirated ABM (n = 7) or heparinized saline (n = 7) was injected transendocardially into the ischemic zone (0.2 ml/injection at 12 sites). Echocardiography to assess myocardial thickening and microspheres to assess perfusion were performed at rest and during stress.

RESULTS

Vascular endothelial growth factor and MCP-1 concentrations increased in a time-related manner. The conditioned medium enhanced, in a dose-related manner, PAEC proliferation. Collateral flow (ischemic/normal zone x 100) improved in ABM-treated pigs (ABM: 98 ± 14 vs. 83 ± 12 at rest, p = 0.001; 89 ± 18 vs. 78 ± 12 during adenosine, p = 0.025; controls: 92 ± 10 vs. 89 ± 9 at rest, p = 0.49; 78 ± 11 vs. 77 ± 5 during adenosine, p = 0.75). Similarly, contractility increased in ABM-treated pigs (ABM: 83 ± 21 vs. 60 ± 32 at rest, p = 0.04; 91 ± 44 vs. 36 ± 43 during pacing, p = 0.056; controls: 69 ± 48 vs. 64 ± 46 at rest, p = 0.74; 65 ± 56 vs. 37 ± 56 during pacing, p = 0.23).

CONCLUSIONS

Bone marrow cells secrete angiogenic factors that induce endothelial cell proliferation and, when injected transendocardially, augment collateral perfusion and myocardial function in ischemic myocardium.

Abbreviations and Acronyms   ABM = autologous bone marrow   BM = bone marrow   H&E = hematoxylin and eosim   LTCM = long-term culture medium   MCP-1 = macrophage chemoattractant protein-1   PAEC = pig aortic endothelial cells   VEGF = vascular endothelial growth factor

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