Cardiovascular effects of inhaled nitric oxide in patients with left ventricular dysfunction

Evan Loh, Jonathon S. Stamler, Joshua M. Hare, Joseph Loscalzo, Wilson S. Colucci

Research output: Contribution to journalArticlepeer-review

189 Scopus citations

Abstract

Background: Pulmonary vascular resistance (PVR) is frequently elevated in patients with advanced heart failure. Nitric oxide (NO), which contributes to the activity of endothelium-derived relaxing factor, causes relaxation of pulmonary arteries and veins in vitro. Inhalation of NO gas causes pulmonary vasodilation in patients with primary and secondary forms of pulmonary hypertension. Methods and Results: To test the hypothesis that inhalation of NO gas lowers PVR in patients with heart failure, we studied the hemodynamic effects of a 10-minute inhalation of NO (80 ppm) in 19 patients with New York Heart Association class III (n=5) and class IV (n=14) heart failure due to left ventricular (LV) dysfunction. Although inhalation of NO had no effect on pulmonary artery pressures, the PVR decreased by 31±7% (P

Original languageEnglish (US)
Pages (from-to)2780-2785
Number of pages6
JournalCirculation
Volume90
Issue number6
StatePublished - Dec 1994
Externally publishedYes

Keywords

  • endothelium-derived factors
  • heart failure
  • lung
  • nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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