Dj. Goldstein et al., INHALED NITRIC-OXIDE IS NOT A NEGATIVE INOTROPIC AGENT IN A PORCINE MODEL OF PULMONARY-HYPERTENSION, Journal of thoracic and cardiovascular surgery, 114(3), 1997, pp. 461-466
Background: Reports of pulmonary edema complicating inhaled nitric oxi
de therapy in patients with chronic heart failure and pulmonary hypert
ension have raised the concern that inhaled nitric oxide may have nega
tive inotropic effects, Methods and results: We investigated the effec
t of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on lef
t ventricular contractile state in 10 open-chest pigs, Pressure-volume
loops were generated during transient preload I eduction to determine
the end-systolic pressure-volume relationship and the stroke work-end
-diastolic volume relation, Inhaled nitric oxide had no effect on syst
emic vascular resistance, cardiac output, end-systolic pressure-volume
relationship or stroke work-end-diastolic volume relation under norma
l conditions, After induction of pulmonary hypertension (intravenous t
hromboxane A(2) analog), inhalation of nitric oxide (80 ppm) resulted
in a reduction in pulmonary vascular resistance (mean +/- standard err
or of the mean) from 10.4 +/- 3 to 6.5 +/- 2 Wood units (p < 0.001) an
d in pulmonary artery pressure from 44 +/- 4 to 33 +/- 4 mm Hg (p < 0.
05). Left ventricular end-diastolic volume rose from 53 +/- 9 mi to 57
+/- 10 mi (p = 0.02), No statistically significant change in cardiac
output or systemic vascular resistance was observed, Inhaled nitric ox
ide had no effect on end-systolic pressure-volume relationship or stro
ke work-end-diastolic volume relation, Conclusions: In a porcine model
of pulmonary hypertension, inhaled nitric oxide does not impair left
ventricular contractile function, Therefore the cause of pulmonary ede
ma observed in some patients receiving inhaled nitric oxide is not due
to a negative inotropic action of this therapy.