Nitric Oxide Synthase Inhibition Weakens Beneficial Effects of Increased Plasma Viscosity on Cardiac Function in Hemodilution Model

Abstract

This study tested the hypothesis that the inhibition of nitric oxide synthase negatively affects the beneficial effects of high viscogenic plasma expander (HVPE) on cardiac performance in a state of hemodilution. Five anesthetized hamsters were administered with N(G)‐nitro‐L‐arginine methyl ester (L‐NAME), nitric oxide synthase inhibitor, as a tested group whereas other five without L‐NAME infusion were used as a control group. Animals were performed an isovolemic hemodilution by 40% of estimated blood volume with dextran 2000 kDa, HVPE with viscosity 6.34 cP. L‐NAME administration followed by isovolemic hemodilution significantly decreased heart rate from 441±41 bpm at baseline to 355±27 bpm at 60 min after hemodilution. End‐systolic pressure increased 14% after L‐NAME infusion and maintained higher than baseline after hemodilution whereas it gradually decreased in animals without L‐NAME infusion. L‐NAME significantly decreased the maximum rate of ventricular pressure change, stroke volume and cardiac output after hemodilution compared to a control group. Systemic vascular resistance increased to 162% and 135% of baseline after L‐NAME infusion and 60 min after hemodilution which is particularly higher than a control group. These results indicate that nitric oxide induced by HVPE play a major role on cardiac function during an isovolemic hemodilution.