Nitric oxide was obtained as a mixture of 900 ppm NO balanced with N2 (Matheson, Rutherford, NJ). The NO/N2 and a N2 source were connected via a soda lime absorber that scavenged nitrogen dioxide (N02) to a gas blender (5100, Bird, Palm Springs, Calif) which allowed the titration of the inspiratory NO concentration. The outlet of the gas blender delivered a NO/N2 gas mixture through the air supply inlet to the high-pressure servo valve of the ventilator that under normal conditions regulated air entry. The two high-pressure servo valves, one for NO/N2 and the other for oxygen, were controlled by the original microprocessor of the ventilator. They opened proportionally, depending on the Vt, flow rate, inspiratory-to-expiratory time ratio, ventilator rate, and FIo2 settings. Nitric oxide and N02 were measured with a chemiluminescence-type NO detector (model 14B/E, Thermo Electron Corp, Franklin, Mass).
After the instrumentation, dogs remained supine. Pulmonary artery blood temperature was kept at 38°C with a heating pad. canadian helth& care mall
Adequate hydration and energy supply (25 kcal/kg/d) was ensured with an infusion of 5 percent dextrose and lactated Ringer’s solution, to achieve a Paotm of 8 mm Hg. Acute lung injury was induced by injection of 0.08 ml/kg of purified oleic acid (J.T. Baker Inc, Phillipsburg, NJ) into the right atrial catheter over 15 min. Additional 0.2-ml increments of oleic acid were administered every 30 min until PaC>2 was between 50 and 60 mm Hg while breathing room air at ambient airway pressure. Then, FI02 was set to 0.3 and the lung injury was allowed to stabilize for 90 min.
Dogs then received, in random order, zero or 40 ppm of NO in the inspiratory gas, with and without 10 cm H2O СРАР. Forty minutes of equilibration were allowed before measurements. To restore lung history, the animals’ lungs were inflated manually to an airway pressure of 30 cm H2O for 10 s after each measurement, before either the inhaled NO concentration or the CPAP level was changed.