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Vascular and Endovascular Surgery
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Allogenic, Multidonor In Vitro Endothelialization of Small Diameter PTFE Grafts in Baboons

Roland Fasol

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

Peter Zilla

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

Petra Preiss

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

Ulrich von Oppell

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

John Odell

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

Bruno Reichart

Department of Cardio-Thoracic Surgery, Groote Schur Hospital, University of Cape Town, Medical School, Cape Town, South Africa

The early effect of allogenic in vitro endothelialization was assessed in small- diameter vascular prostheses. Cryopreserved and pooled venous endothelial cells (ECs) from 13 baboons of similar blood group were used for confluent in vitro endothelialization of fibrin glue-coated polytetrafluoroethylene vascular grafts. Bilateral femoral interpositions (12 cm) of experimental and control grafts were subsequently implanted into a separate group of 18 male baboons with the same blood group as that of the pooled cells. After sixteen days of implantation the patency rate of grafts of the endothelialized group was similar to that of the control group (55.6% vs 61.1%, p>0.1). Scanning electron microscopy revealed that 44.4% of experimental grafts were completly free of endothelium, while the remaining grafts showed a moderate mean EC coverage of 34.4 17.1%. These remaining ECs were found mainly as small islands densely covered by leukocytes. The majority of these white cells resembled granulocytes, although adherent lymphocytes were also regularly observed. Since surface morphology does not explain the mechanism of EC loss, further experiments must elucidate this question.

If rejection is found to be the primary cause for this cell loss, the use of major histocompatibility complex (MHC) matched EC subpools might be considered.

Vascular and Endovascular Surgery, Vol. 25, No. 1, 64-71 (1991)
DOI: 10.1177/153857449102500111


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