Abstract
Angiogenesis is a complex phenomenon consisting of several distinct processes which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling (1). Although an increasing body of evidence has accumulated regarding to in vitro biological activities of different growth factors and related peptides as well as their roles during in vitro angiogenesis, very little is known about the mechanisms of coronary angiogenesis in the ischemic heart. In 1971, Schaper et al (2) first demonstrated that the enlargement of preexisting coronary anastomoses, mostly of arteriolar size, was accompanied by proliferative activities, i.e. DNA synthesis, of vascular endothelial cells in dogs subjected to chronic left circumflex arterial occlusion. This was later shown to be true also in ischemic porcine hearts, where endothelial cells of various sizes of vessels were found to be proliferating, most prominent at the capillary level (3,4). These findings have led us to the recognition that coronary collateral development is much more than a simple mechanical dilatation of native anastomotic channels. This chapter will focus mainly on microvascular adaptations that are commonly developed in ischemic porcine and human hearts.
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Mohri, M., Schaper, W. (1992). Angiogenesis in Porcine Hearts with Coronary Microembolization. In: Schaper, W., Schaper, J. (eds) Collateral Circulation. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3092-3_6
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DOI: https://doi.org/10.1007/978-1-4615-3092-3_6
Publisher Name: Springer, Boston, MA
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