Impacts of pulsatile systemic circulation on endothelium-derived nitric oxide release in anesthetized dogs.

Abstract

The effects of pulsatile flow on endothelium-derived nitric oxide-mediated vasodilation are not fully elucidated in an in vivo model. A left ventricular assist device was established in 10 anesthetized dogs with a centrifugal pump and an air-driven pneumatic pump. The systemic circulation was subjected to step changes in the frequency of pulse (0, 30, 60, and 120 bpm with a fixed pulse pressure of 50 mm Hg), and in the amplitude of pulse (0, 20, and 50 mm Hg with a fixed pulse rate of 120 bpm). Hemodynamic variables and calculated total systemic vascular resistance were compared before and after the administration of N(G)-Nitro-L-arginine Methyl Ester (L-NAME) (20 mg/kg). Plasma NO2-/NO3- concentration levels were also measured. Total systemic vascular resistance significantly decreased while plasma NO2-/No3- concentration increased in response to the rise in both pulse rate and pulse pressure. However, L-NAME significantly diminished these effects of pulsatile flow. Both the frequency and the amplitude of pulse wave in the systemic circulation are significant independent stimuli for endothelium-derived nitric oxide-mediated vasodilation in vivo.