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Ann Thorac Surg 2001;72:156-162
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

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

Toshihide Nakano, MDa, Ryuji Tominaga, MDa, Shigeki Morita, MDa, Munetaka Masuda, MDa, Ichiro Nagano, MDa, Ken-ichi Imasaka, MDa, Hisataka Yasui, MDa a Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan

Accepted for publication March 15, 2001.

Address reprint requests to Dr Tominaga, Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582 Japan
e-mail: tomina{at}heart.med.kyushu-u.ac.jp

Background. The effects of pulsatile flow on endothelium-derived nitric oxide-mediated vasodilation are not fully elucidated in an in vivo model.

Methods. 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 NG-Nitro-L-arginine Methyl Ester (L-NAME) (20 mg/kg). Plasma NO2-/NO3- concentration levels were also measured.

Results. 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.

Conclusions. 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.




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