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Updated: Jan 31, 2026
10:31
Surgical Angiogenesis in Porcine Tibial Allotransplantation: A New Large Animal Bone Vascularized Composite Allotransplantation Model
Published on: August 13, 2017
8.0K
A Flow Dynamic Rationale for Accelerated Vascularized Composite Allotransplant Rejection.
Nicholas L Robbins1, Matthew J Wordsworth1, Bijaya K Parida1
1From the RESTOR Program, 59th Medical Wing, and the San Antonio Military Medical Center, Joint Base San Antonio; University of Texas Health at San Antonio; Baylor Scott & White Health; and the Wake Forest Institute for Regenerative Medicine.
Plastic and Reconstructive Surgery
|January 10, 2019
Summary
Vascularized composite allotransplants using long donor arteries (over 25 cm) experienced accelerated failure due to chronic rejection. This study suggests ischemia and intimal hyperplasia disrupt the Windkessel effect, leading to transplant loss.
Area of Science:
- Vascular surgery
- Transplant immunology
- Histopathology
Background:
- Six knee and one hand vascularized composite allotransplants (VCAs) utilized donor arteries 25-40 cm long.
- All VCAs failed between 14-56 months, attributed to chronic rejection.
- A hand transplant failure at 8 months showed arterial pedicle thickening, intimal hyperplasia, and near "no-flow phenomenon" without cutaneous rejection.
Purpose of the Study:
- To investigate the cause of accelerated failure in VCAs using long donor arterial pedicles.
- To analyze the role of T-cell-mediated rejection and ischemia in VCA graft survival.
Main Methods:
- Retrospective analysis of seven published VCA cases using donor arteries >25 cm.
- Data collected from transplant teams in Germany and Louisville, Kentucky.
- Outcome measures included transplant survival time and histopathologic findings.
Main Results:
- A 100% accelerated failure rate was observed in VCAs with donor arteries >25 cm.
- Graft loss was linked to T-cell-mediated rejection and ischemia-induced arterial necrosis.
- Histopathology revealed intimal hyperplasia and disruption of the Windkessel effect.
Conclusions:
- Hypothesizes accelerated rejection due to ischemia from disrupted vasa vasorum and intimal hyperplasia.
- Suggests intimal hyperplasia, exacerbated by ischemia, disrupts the Windkessel effect, causing expedited transplant failure.
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