The minimal dose of FK506 is sufficient to facilitate the arterialisation of venous allografts in rats

Abstract

Background We investigated whether a minimal dose of FK506 is sufficient to inhibit the rejection of venous allografts and facilitate allograft adaptation to arterialisation in rats.Methods Iliolumbar veins from Brown Norway (BN) rats were transplanted into the abdominal aorta of Lewis (LEW) rats. Recipient animals received daily intramuscular injections of 0.1 mg kg −1 FK506. Light microscope evaluations of grafts were performed 30 days after transplantation. We investigated the presence of endothelial cells, the intensity of intimal proliferation, the deposition of immunoglobulin G molecules into the medial layer and the degree of adventitial infiltration by Lewis MHC class II-positive, CD4-positive and CD8-positive cells. All results were compared to previously reported data for syngeneic, allogeneic non-immunosuppressed and allogeneic FK506-low-dose immunosuppressed animals.Results All alloveins under minimal FK506 immunosuppression showed typical histological signs of arterialisation 30 days after transplantation. Intimal thickness (15.1 ± 6.1 µm) and the degree of adventitial infiltration by MHC class II-positive (16.96 ± 10.46), CD8-positive (2.63 ± 2.6), and CD4-positive (7.67 ± 8.29) cells were not significantly different when compared to untreated syngeneic veins and allogeneic veins treated with a low dose of FK506, respectively.Conclusions Even the minimal dose of FK506 was sufficient to inhibit the acute rejection of venous allografts and to facilitate allograft arterialisation 30 days after transplantation.

Response of Endothelial Cells to Gelatin-Based Hydrogels

“…6 Moreover, the mismatch in mechanical properties between the elastic native artery and the rigid devices might induce proliferation of vascular smooth muscle cellsleading to hyperplasia and possibly ending up with vascular stenosis/occlusion. 7,8 Failure of cardiovascular implants can best be avoided by adjusting the elastic modulus of the implant to the surrounding tissue together with the growth of a functionally confluent monolayer of endothelial cells on the luminal surface. To establish such a cell monolayer on polymer surfaces, optimal adhesion and spreading of the cells are desired.…”

“…Cardiovascular devices therefore can fail, in part, due to thrombosis resulting from the lack of endothelium . Moreover, the mismatch in mechanical properties between the elastic native artery and the rigid devices might induce proliferation of vascular smooth muscle cellsleading to hyperplasia and possibly ending up with vascular stenosis/occlusion. , …”