Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs.

Abstract

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/nitrite production during a VAI. Prospective trial. University laboratory. Anesthetized mongrel dogs received a VAI (0.2 ml 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 immunosorbent assay) and nitrate/nitrite (by high-performance liquid chromatography) levels. The cardiac index increased 24 % and the pulmonary vascular resistance index decreased 30 % during both periods of NO inhalation. Arterial oxygen tension and arterial oxygen saturation were slightly lower after NO therapy. Nitrate/nitrite concentrations were unaltered in the control group and there were no differences between the arterial and mixed venous serum nitrate/nitrite levels. Nitrite concentrations remained below 1 microM in both groups 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 group, but there was no increase in NO-treated animals (all p < 0.05) Nitrate/nitrite concentrations were unaltered after VAI in dogs. NO therapy attenuated TxA(2) release and improved hemodynamics, but not blood oxygenation, in dogs with a VAI. There were no differences between the responses to 3 ppm and 40 ppm NO.