NITRIC-OXIDE MEDIATES THE HYPERTENSIVE RESPONSE TO A MODIFIED HEMOGLOBIN SOLUTION (DCLHB(TM)) IN RATS

We investigated the effect of nitric oxide synthase inhibition with L-NAME, and of L-arginine (nitric oxide synthase substrate), on the hemodynamic response to a modified hemoglobin solution (DCLHb). Rats were given one of the following regimens (all groups hypervolemic except Control): Control-8.0 ml of donor blood (isovolemic exchange); HV-8.0 ml of donor blood; DCLHb-8.0 ml of DCLHb, L-NAME-30 mg kg(-1) of L-NAME followed by 8.0 ml of DCLHb; or L-Arg-8.0 ml of DCLHb followed by Larginine (600 mg.kg(-1)). Mean arterial blood pressure (MABP) was continuously recorded and the change compared to baseline and expressed as Delta MABP. Delta MABP was greater in the HV and DCLHb groups versus the Control and L-NAME groups; and was greater in the DCLHb group Versus the HV group. Delta MABP was not different between the Control and L-NAME group. In the L-Arg group the initial Delta MABP (after DCLHb) was similar to the DCLHb group; however, after L-arginine administration Delta MABP was not different from the Control group. This study supports a hypothesis that DCLHb effects an increase in MABP by a nitric oxide related mechanism.