Recorded presentation.
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 in the warming process of induced hypothermia after a major cardiac event. Nitric oxide (NO) was introduced through sodium nitrate which was aimed to reduce the speed and turbulence of blood flow. 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 process of induced hypothermia, and three concentrations of sodium nitrate were added to the samples. A control was used for comparison and for calculations. 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
