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Vol. 84, Issue 2, 435-441, February 1998
1 Department of Anesthesia and Critical Care, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02114; and 2 National Cancer Institute, Frederick, Maryland 21702
Adrie, Christophe, Fumito Ichinose, Alexandra
Holzmann, Larry Keefer, William E. Hurford, and Warren M. Zapol. Pulmonary vasodilation by nitric oxide gas and prodrug
aerosols in acute pulmonary hypertension. J. Appl. Physiol. 84(2): 435-441, 1998.
Sodium 1-(N,N-diethylamino)diazen-1-ium-1,2-diolate
{DEA/NO;
Et2N[N(O)NO]Na} is a compound that spontaneously generates nitric oxide (NO). Because
of its short half-life (2.1 min), we hypothesized that inhaling DEA/NO
aerosol would selectively dilate the pulmonary circulation without
decreasing systemic arterial pressure. We compared the pulmonary
selectivity of this new NO donor with two other reference drugs:
inhaled NO and inhaled sodium nitroprusside (SNP). In seven awake sheep
with pulmonary hypertension induced by the infusion of U-46619, we
compared the hemodynamic effects of DEA/NO with those of incremental
doses of inhaled NO gas. In seven additional awake sheep, we examined
the hemodynamic effects of incremental doses of inhaled nitroprusside
(i.e., SNP). Inhaled NO gas selectively dilated the pulmonary
vasculature. Inhaled DEA/NO produced nonselective vasodilation; both
systemic vascular resistance (SVR) and pulmonary vascular resistance
(PVR) were reduced. Inhaled SNP selectively dilated the pulmonary
circulation at low concentrations
(
10
2 M), inducing a
decrease of PVR of up to 42% without any significant decrease of SVR
(
5%), but nonselectively dilated the systemic circulation at
larger doses (>102 M). In
conclusion, despite its short half-life, DEA/NO is not a selective
pulmonary vasodilator compared with inhaled NO. Inhaled SNP appears to
be selective to the pulmonary circulation at low doses but not at
higher levels.
nitric oxide adducts; sodium nitroprusside; sheep
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