THE EFFECT OF HYPOCAPNIA AND MECHANICAL PULMONARY STRESS ON LUNG-TISSUE IN NEWBORN LAMBS

Positive pressure ventilation, using high inspiratory pressures, often causes lung damage. When associated with hypocapnia, it can produce s evere focal alveolar alkalosis and can cause damage in areas of low bl ood flow. A vein-to-vein extracorporeal membrane oxygenator (ECMO) sys tem was used to control blood gases independently of mechanical ventil ation in 12 healthy newborn lambs. After connection to the ECMO system , ventilation was started with a peak inspiratory pressure of 35 cm H2 O and a positive end-expiratory pressure of 5 cm H2O; the ventilator r ate was 40/min with I:E = 1.5 and FiO2 = 1.0. In 6 of the 12 lambs swe ep gases through the silicone membrane were regulated to assure arteri al normocapnia. The other 6 were ventilated with the same settings and perfused with the same pump flow, but PaCO2 was allowed to fall to hy pocapnic levels. The lambs were ventilated for 4 h. Average pH and PaC O2 were 7.62 +/- 0.14 and 2.11 +/- 0.54 kPa, respectively, in the hypo capnic group and 7.39 +/- 0.11 and 4.79 +/- 0.51 kPa in the normocapni c group. After sacrificing the lambs, the lungs were inspected macrosc opically and microscopically by computer-assisted morphometry to asses s atelectasis and lung edema. Macroscopically there were no hemorrhage s, barotrauma or widespread atelectasis of the lungs in either group. The thickness of interlobular lung septa in the right upper lobe was 3 2.5 +/- 18.0 mum for the hypocapnic group and 29.7 +/- 12.5 mum for th e normocapnic group. The parenchymal-alveolar area ratio in the right upper lobe was 28.4 +/- 5.04 and 24.6 +/- 3.75% in the hypocapnic and normocapnic groups, respectively. Hypocapnia and mechanical stress for 4 h in initially healthy lungs did not produce alveolar epithelial da mage.