Abstract
Objective: We examined the molecular mediators of postoperative choke-vessel growth. Our focus was the possible overlap between choke-vessel growth and arteriogenesis.
Methods: A rat perforator flap model, encompassing four vascular territories, was used. Flaps were surgically elevated, re-inset, and allowed to survive for one, three, five, or seven days. Tissue samples for Western and histological analyses were collected from the choke zone along the dorsal midline. Tissue from territories linked by the choke zone was analyzed to distinguish between global and local effects. The proteins examined included CD11b, ICAM-1, and MMP-2, three markers associated with arteriogenesis, as well as Hsp70 and vascular endothelial growth factor, markers of physiological stress and hypoxia/ischemia.
Results: Arteriogenesis markers, as shown by Western analysis, increased at three and five days after flap elevation, and the increase was localized by immunohistochemistry to the growing arteries and veins. The marker of physiological stress increased at Days 5 and 7. The hypoxia-ischemia marker did not increase in the choke zone.
Conclusions: The growth of choke arteries and veins proceeds in an inflammatory environment that resembles arteriogenesis. Ischemia did not appear to play a role in choke-vessel changes.
Acknowledgements
The authors thank Dr. Frank Smith (PhD) for helpful suggestions on the paper, Kathleen Murphy for her excellent technical assistance, and Dr. Roger Croll (PhD) for a gift of fluorescent phalloidin. B.A.W. had a scholarship from the Natural Sciences and Engineering Research Council, and the research was funded by the Capital Health Research Foundation, Dalhousie University Department of Surgery, and Heart and Stroke Foundation of New Brunswick.