P. Dahm et al., CIRCULATORY AND VENTILATORY EFFECTS OF INTERMITTENT NITRIC-OXIDE INHALATION DURING PORCINE ENDOTOXEMIA, The journal of trauma, injury, infection, and critical care, 37(5), 1994, pp. 769-777
The effects of intermittent inhalation of 57 ppm nitric oxide (NO) wer
e studied in eight anesthetized, ventilated pigs given a continuous in
fusion of Escherichia coli endotoxin. Seven animals served as controls
. By administering NO synchronized with inspiration and close to the o
rotracheal tube, measurable amounts of the toxic metabolite, NO2, in t
he inspiratory gas mixture were avoided. No direct systemic effects of
NO inhalation were seen, but through counteracting pulmonary vasocons
triction, a fall in cardiac output was delayed. Nitric oxide effective
ly attenuated the initial peak rise in mean pulmonary artery pressure
and resistance, both returning to control levels after cessation of NO
. These effects were reproduced during later phases of endotoxemia, gi
ving further proof to the role of gaseous NO as a selective pulmonary
vasodilator. Nitric oxide diminished pulmonary shunting, but unimpaire
d oxygenation Was preserved only during the first inhalation period. L
eukocyte counts decreased drastically and platelet aggregation was enh
anced, but after 1.5 hours of endotoxin infusion, platelet hyperaggreg
ation was maintained in the NO group while it decreased in the control
group.