Abstract
Background: The use of immunosuppresants such as cyclosporin (CyA) has been linked to the development of accelerated cardiac allograft vasculopathy (CAV). CyA may promote CAV by (i) impairing nitric oxide (NO) mediated vasodilatation, (ii) stimulating oxidant production and (iii) downregulating Fas-Ligand (FasL) expression thereby leading to neutrophil migration. In the present study, we hypothesized that the NO synthase cofactor, tetrahydrobiopterin (BH4), would attenuate the deleterious effects of CyA via the aforementioned pathways.
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