title: The Formation of Aberrant Collateral Vessels during Coronary Arteriogenesis in Dog Heart.
abstract: We previously reported excessive growth of collateral vessels in the dog heart during arteriogenesis induced by implantation of an ameroid constrictor around the circumflex branch of the left coronary artery. In the present study, using histology and immunocofocal microscopy, we further investigated how these aberrant collateral vessels form. By comparison with mature collateral vessels the following findings were made: perivascular space was very narrow where damage of the perivascular myocardium occurred; the neointima was very thick, resulting in a very small lumen; elastica van Gieson staining revealed the absence of the internal elastic lamina and of elastic fibers in the adventitia, but abundant collagen in the adventitia as well as in the neointima; smooth muscle cells of the neointima expressed less α-SM actin and little desmin; expression of the fibroblast growth factors aFGF, bFGF and platelet-derived growth factor (PDGF)-AB was observed mainly in the endothelial cells and abluminal region, but transforming growth factor-β1 was only present in the adventitia and damaged myocardium; angiogenesis in the neointima was observed in some collateral vessels expressing high levels of eNOS, and cell proliferation was mainly present in the abluminal region, but apoptosis was in the deep neointima. In conclusion, these data for the first time reveal that the formation of the aberrant collateral vessels in the dog heart involves active extracellular proteolysis and a special expression profile of growth factors, eNOS, cell proliferation and apoptosis. The finding of a narrow perivascular space and perivascular myocardial damage suggests that anatomical constraint is most likely the cause for exacerbated inward remodeling in aberrant collateral vessels in dog heart.
authors.affiliation: Department of Histology and Embryology, School of Basic Medicine, Central South University Changsha, Hunan, PR China.
authors.forename: Yinglu
authors.initials: Y
authors.lastname: Guan
authors.forename: Baizhen
authors.initials: B
authors.lastname: Cai
authors.forename: Zhenghua
authors.initials: Z
authors.lastname: Liu
authors.forename: Feng
authors.initials: F
authors.lastname: Ye
authors.forename: Panyue
authors.initials: P
authors.lastname: Deng
authors.forename: Wei-Jun
authors.initials: WJ
authors.lastname: Cai
authors.forename: Jutta
authors.initials: J
authors.lastname: Schaper
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schaper
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D017209:Apoptosis; D049109:Cell Proliferation; D054059:Coronary Occlusion / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology*; D003893:Desmin / Q000032:analysis; D004285:Dogs; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis; D009206:Myocardium / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000473:pathology / Q000503:physiopathology*; D052250:Nitric Oxide Synthase Type III / Q000032:analysis
chemical_list: D000199:Actins; D003893:Desmin; D036341:Intercellular Signaling Peptides and Proteins; D052250:Nitric Oxide Synthase Type III