Tetrahydrobiopterin in Ischemia and Reperfusion Injury : a murine heart transplantation model

The essential co-factor of endothelial nitric oxide synthase (eNOS) tetrahydrobiopterin (BH4) has been repeatedly shown to protect transplanted organs from ischemia reperfusion injury (IRI). So far, the underlying mechanism has not been described. One hypothesis is that BH4 treatment prevents disruption of the functional nitric oxide producing form of eNOS, the so-called "uncoupling" and related superoxide production, by sustaining the dimeric status of the enzyme. Herein we tested this hypothesis in a murine transplantation model.