Inhaled nitric oxide prevents left ventricular impairment during endotoxemia

Satoshi Ishihara, John A. Ward, Osamu Tasaki, Basil A. Pruitt, Cleon W. Goodwin, David W. Mozingo, William G. Cioffi

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


We evaluated the effect of long-term inhalation of nitric oxide (NO) on cardiac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to measure LV volume and a micromanometer to measure LV pressure. One week later, the animals were divided into a control group (n = 6) or a NO group (n = 6). All animals received intravenous Escherichia coli endotoxin (10 μg·kg-1·h-1) and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The end-systolic elastance in the control group was significantly decreased beyond 7 h. NO inhalation maintained the end-systolic elastance at baseline levels and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.

Original languageEnglish (US)
Pages (from-to)2018-2024
Number of pages7
JournalJournal of applied physiology
Issue number6
StatePublished - Dec 1998


  • Cardiac contractility
  • Endotoxin
  • Hemodynamics
  • Left ventricular function
  • Nitric oxide inhalation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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