Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure

M. Argenziano, D. A. Dean, N. Moazami, Daniel J. Goldstein, E. A. Rose, H. M. Spotnitz, D. Burkhoff, M. C. Oz, M. L. Dickstein

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background: Inhaled nitric oxide has been shown to be a potent and selective pulmonary vasodilator. Reports of increases in left ventricular end-diastolic pressure and episodes of pulmonary edema during the clinical use of inhaled nitric oxide in patients with preexisting left ventricular dysfunction have raised concerns that this agent may have myocardial depressant effects. We therefore undertook a study of the effects of inhaled nitric oxide on myocardial contractility in a porcine model of ventricular failure and pulmonary hypertension. Methods: After inducing heart failure in 10 pigs by rapid ventricular pacing, hemodynamic measurements and pressure- volume diagrams (by the conductance method) were obtained in six animals at baseline and during administration of inhaled nitric oxide at concentrations of 20 and 40 ppm. Myocardial contractile state was assessed by the end- systolic pressure-volume relationship and preload-recruitable stroke work, whereas diastolic function was measured in terms of the end-diastolic pressure-volume relationship and the pressure decay time constant T. Results: Baseline hemodynamics reflected heart failure and pulmonary hypertension, and inhaled nitric oxide induced significant reductions in mean pulmonary artery pressure and pulmonary vascular resistance. Although left ventricular end- diastolic pressure increased during administration of inhaled nitric oxide, no changes were observed in measures of systolic or diastolic function. Conclusions: Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function. Increases in left ventricular end-diastolic pressure during inhaled nitric oxide therapy are therefore not due to myocardial depression and may be related to increases in volume delivery to the left side of the heart resulting from reduced pulmonary vascular resistance.

Original languageEnglish (US)
Pages (from-to)700-708
Number of pages9
JournalJournal of Thoracic and Cardiovascular Surgery
Volume115
Issue number3
DOIs
StatePublished - 1998
Externally publishedYes

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Anti-Arrhythmia Agents
Nitric Oxide
Swine
Heart Failure
Blood Pressure
Vascular Resistance
Pulmonary Hypertension
Pressure
Hemodynamics
Left Ventricular Dysfunction
Pulmonary Edema
Theophylline
Vasodilator Agents
Pulmonary Artery
Stroke
Lung

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure. / Argenziano, M.; Dean, D. A.; Moazami, N.; Goldstein, Daniel J.; Rose, E. A.; Spotnitz, H. M.; Burkhoff, D.; Oz, M. C.; Dickstein, M. L.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 115, No. 3, 1998, p. 700-708.

Research output: Contribution to journalArticle

Argenziano, M, Dean, DA, Moazami, N, Goldstein, DJ, Rose, EA, Spotnitz, HM, Burkhoff, D, Oz, MC & Dickstein, ML 1998, 'Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure', Journal of Thoracic and Cardiovascular Surgery, vol. 115, no. 3, pp. 700-708. https://doi.org/10.1016/S0022-5223(98)70336-8
Argenziano, M. ; Dean, D. A. ; Moazami, N. ; Goldstein, Daniel J. ; Rose, E. A. ; Spotnitz, H. M. ; Burkhoff, D. ; Oz, M. C. ; Dickstein, M. L. / Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure. In: Journal of Thoracic and Cardiovascular Surgery. 1998 ; Vol. 115, No. 3. pp. 700-708.
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