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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00478.2002
Submitted on June 7, 2002
Accepted on August 23, 2002
1 Department of Anatomy, Hunan Medical University, Hunan, China; Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany
2 National Institute of Cardiology, Budapest, Hungary
3 Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany
4 Department of Anatomy, Hunan Medical University, Hunan, China
* To whom correspondence should be addressed. E-mail: j.schaper{at}kerckhoff.mpg.de.
We studied the role of the adventitia in adaptive arteriogenesis during the phase of active growth of coronary collateral vessels (CV) induced by chronic occlusion of the left circumflex coronary artery in canine hearts. We used electron microscopy and immunoconfocal (IF) labeling for bFGF, matrix metallo-proteinases 2 (MMP-2), MMP-9, tissue-type plasminogen activator (t-PA), its inhibitor-1 (PAI-1), fibronectin (FN) and Ki-67. Proliferation of smooth muscle cells and adventitial fibroblasts was evident. Quantitative IF showed that adventitial MMP-2, MMP-9 and FN were 9.2-fold, 7.5-fold and 8.6-fold, bFGF 5.1 fold and PAI-1 3.4 fold higher in CV than in normal vessels (NV). The number of fibroblasts was 5-fold elevated in CV but the elastic fiber content was 25-fold greater in NV than in CV. Perivascular myocyte damage and induction of eNOS in peri-CV capillaries indicate expansion of CV. It is concluded that adventitial activation is associated with the development of CV through cell proliferation, production of growth factors, and induction of extracellular proteolysis thereby contributing to remodeling during adaptive arteriogenesis.
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