Nitric oxide does not play a major role in the regulation of systemic hemodynamic responses to acute normovolemic hemodilution

Background: The mechanisms of cardiovascular changes following acute normov olemic hemodilution (ANH) have not been fully elucidated. We tested the hyp othesis that inhibition of nitric oxide synthesis attenuates ANH-induced ca rdiovascular responses. Methods: We observed the effects of N-omega-nitro-L-arginine methyl ester ( L-NAME) pretreatment on ANH-induced cardiovascular responses and compared t hese effects with those elicited by phenylephrine (PHE). Twenty dogs anesth etized with isoflurane were divided into two groups: one group was pretreat ed with L-NAME and the other with PHE. Both groups were normovolemically he modiluted using 6% hydroxyethyl starch to reduce the hemoglobin concentrati on to approximately 50% of the pretreatment value. Results: Pretreatment with either L-NAME or PHE caused a significant increa se in mean aortic blood pressure (MAP) and systemic vascular resistance (SV R) with a significant decrease in cardiac output (CO) and stroke volume (SV ). However, no remarkable differences in these variables were seen between groups. In both groups ANH produced increases in heart rate, CO, SV, and ma ximal left ventricular dP/dt with a significant decrease in SVR. No signifi cant differences in these variables were apparent after ANH except that MAP was decreased in the PHE group but not in the L-NAME group. Conclusion: Our results suggest that nitric oxide does not play a major rol e in mediation or modulation of the systemic vascular responses to ANH.