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Related Experiment Videos

Effect of inhaled nitric oxide on normal human left ventricular function

C S Hayward1, W V Kalnins, P Rogers

  • 1Cardiology Department, St. Vincent's Hospital, Darlinghurst, New South Wales, Australia.

Journal of the American College of Cardiology
|July 1, 1997
PubMed
Summary

Inhaled nitric oxide (NO) at 20 ppm did not affect normal human left ventricular (LV) function. Rapid inactivation of NO before reaching the heart may explain this lack of effect on LV contractility.

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Area of Science:

  • Cardiovascular Physiology
  • Pulmonary Medicine
  • Pharmacology

Background:

  • Inhaled nitric oxide (NO) is a selective pulmonary vasodilator.
  • In heart failure, NO can increase pulmonary capillary wedge pressure.
  • Potential negative inotropic effects of NO on left ventricular (LV) function are unknown when inhaled.

Purpose of the Study:

  • To determine the effects of inhaled nitric oxide (NO) on load-independent indexes of normal human left ventricular (LV) function.

Main Methods:

  • Eleven subjects with normal LV function underwent pressure-volume loop recordings.
  • Left ventricular (LV) function was assessed using end-systolic and end-diastolic pressure-volume and preload recruitable stroke work relations.
  • Nitric oxide (NO) was delivered at 20 ppm for 10 minutes; pulmonary vascular resistance (PVR) and NO metabolites were also measured.

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Main Results:

  • Inhaled nitric oxide (NO) did not alter steady-state LV pressures, volumes, contractility, relaxation, or compliance.
  • Pulmonary vascular resistance (PVR) remained unchanged.
  • NO metabolites were detected in the LV cavity, suggesting rapid inactivation before reaching the heart.

Conclusions:

  • Inhaled nitric oxide (NO) at 20 ppm does not significantly affect normal left ventricular (LV) function.
  • Rapid inactivation of inhaled NO in transit to the heart may be responsible for the observed lack of effect on LV function.