Objective: To evaluate the hemodynamic effects of inhaled nitric oxide (NO)
during a venous air infusion (VAI) in dogs. We also addressed the question
of whether NO therapy changes thromboxane (Tx) A(2) release and nitrate/ni
trite production during a VAI.
Design: Prospective trial.
Setting: University laboratory.
Interventions: Anesthetized mongrel dogs received a VAI (0.2 mi x kg(-1) x
min(-1)) after the measurement of baseline hemodynamics. Control dogs (n =
8) received no further treatment. After 30 min of VAI, NO 3 ppm inhalation
was initiated (n = 7) for 30 min, followed by 30 min without NO inhalation,
and then a final 30 min of NO 40 ppm treatment. Hemodynamic variables were
registered and arterial and mixed venous blood samples were drawn for gas
analysis and for the determinations of serum TxB(2) (by enzyme-linked immun
osorbent assay) and nitrate/nitrite (by high-performance liquid chromatogra
phy) levels.
Results: The cardiac index increased 24% and the pulmonary vascular resista
nce index decreased 30 % during both periods of NO inhalation. Arterial oxy
gen tension and arterial oxygen saturation were slightly lower after NO the
rapy. Nitrate/nitrite concentrations were unaltered in the control group an
d there were no differences between the arterial and mixed venous serum nit
rate/nitrite levels. Nitrite concentrations remained below 1 mu M in both g
roups of animals, but the nitrate concentration increased after inhalation
of 40 ppm NO. Serum TxB(2) increased after 60 min of VAI in the control gro
up, but there was no increase in NO-treated animals (all p < 0.05)
Conclusions: Nitrate/nitrite concentrations were unaltered after VAI in dog
s. NO therapy attenuated TxA(2) release and improved hemodynamics, but not
blood oxygenation, in dogs with a VAI. There were no differences between th
e responses to 3 ppm and 40 ppm NO.