The human body has natural systems for vasodilation which are fueled by nitric oxide production, but in cases of cardiac disfunction and stress nitric oxide can be inhibited. In this study, nitric oxide was studied as a mediator for the blood rush experienced from the warming after induced hypothermia. Nitric oxide (NO) was introduced through sodium nitrate, which was aimed to reduce the speed and turbulence of blood flow through interaction between NO and the active site of hemoglobin. A viscometer was used to examine the rate of blood flow, while the temperature was varied to simulate the conditions of induced hypothermia. Two temperatures were tested to simulate the warming following induced hypothermia, and three concentrations of sodium nitrate were added to the samples to examine the correlation between flow and concentration. The results indicated that the 0.11 M NaNO3 expressed constant blood viscosity for both temperatures, the 0.09 M NaNO3 exhibited some mediation, and the 0.10 M showed the least mediation. Therapeutic Hypothermia Therapeutic cooling has been employed in medicine for a very long time, but with varied results. In recent years, several studies have examined induced hypothermia as a treatment after cardiac arrest. These studies have concluded that cooling patients slows tissue damage caused from cardiac trauma [1,2]. Therapeutic hypothermia, however, contributes to a high mortality