Circulation, Vol 83, 2038-2047, Copyright © 1991 by American Heart Association
C Frostell, MD Fratacci, JC Wain, R Jones and WM Zapol
Background. The gas nitric oxide (NO) is an important endothelium- derived
relaxing factor, inactivated by rapid combination with heme in hemoglobin.
Methods and Results. Awake spontaneously breathing lambs inhaled 5-80 ppm
NO with an acutely constricted pulmonary circulation due to either infusion
of the stable thromboxane endoperoxide analogue U46619 or breathing a
hypoxic gas mixture. Within 3 minutes after adding 40 ppm NO or more to
inspired gas, pulmonary hypertension was reversed. Systemic vasodilation
did not occur. Pulmonary hypertension resumed within 3-6 minutes of ceasing
NO inhalation. During U46619 infusion pulmonary vasodilation was maintained
up to 1 hour without tolerance. In the normal lamb, NO inhalation produced
no hemodynamic changes. Breathing 80 ppm NO for 3 hours did not increase
either methemoglobin or extravascular lung water levels nor modify lung
histology compared with control lambs. Conclusions. Low dose inhaled NO
(5-80 ppm) is a selective pulmonary vasodilator reversing both hypoxia- and
thromboxane-induced pulmonary hypertension in the awake lamb [corrected].
ARTICLES
Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction [published erratum appears in Circulation 1991 Nov;84(5):2212]
Department of Anesthesia, Harvard Medical School, Massachusetts General Hospital, Boston.
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