How to protect liver graft with nitric oxide

Figure 4 Modulation of the decline in endothelial nitric oxide synthase-derived nitric oxide production. endothelial nitric oxide synthase (e-NOS)-derived nitric oxide (NO) bioavailability can be compromised either by a reduced L-arginine and cofactor (tetrahydrobiopterin, BH4) availability, or by a decreased e-NOS protein activity and level. Two ways seem to be able to overcome these obstacles: the use of exogenous sources of NO (NO donors or NO inhalation) and the induction of the endogenous downstream effectors of e-NOS (pharmacological treatment or ischemic preconditioning) or transfection by an adenovirus containing e-NOS enzyme. SNP: Sodium nitroprusside; GSNO: S-nitroso-L-glutathione; AICAR: 5-amino-4-imidazole carboxamide riboside; TMZ: Trimetazidine; APC: Activated protein C; AMPK: Adenosine monophosphate protein kinase; PI3K: Phosphoinositide 3-kinase.