Nitric oxide (NO) is an endogenous antibacterial agent produced by immune cells in response to pathogens. Herein, the NO fluxes necessary to reduce bacterial adhesion of different bacteria (S. aureus, methicillin-resistant S. aureus, S. epidermidis, E. faecalis, E. coli, and P. aeruginosa) were investigated to ascertain the sensitivity of these bacteria to NO. S-nitrosothiol NO donor-modified xerogels were selected as a model NO-release surface due to their extended NO-release kinetics relative to other NO donor systems. The xerogels were coated with poly(vinyl chloride) (PVC) to achieve consistent surface energy between NO-releasing and control substrates. Fibrinogen was pre-adsorbed to these materials to more accurately mimic conditions encountered in blood and promote bacteria adhesion. Nitric oxide fluxes ranging from 20-50 pmol cm-2 s-1 universally inhibited the bacterial adhesion by >80% for each strain studied. Maximum bacteria killing activity (reduced viability by 85-98%) was observed at the greatest NO payload (1700 nmol cm-2).