Abstract
Anesthetized young rabbits were ventilated for 6 hr at 20 cm H2O peak airway pressure using air nebulized with water at 22 degrees C (cold nebulized group, n = 11), at 36 degrees C (warm nebulized group, n = 11) and humidified air at 36 degrees C (warm humidified group, n = 10). Their biochemical status during ventilation and pulmonary morphology at autopsy were compared to those of ten control rabbits. Both nebulized groups had particulate water in the inspired air and water of condensation in the endotracheal tube. The rabbits ventilated with warm humidified air and the control group breathing spontaneously maintained their blood pressure and pHa within physiologic range. Rabbits ventilated with air nebulized with water at 22 and 36 degrees C had a significant decline in mean blood pressure (96 mm Hg leads to 61 mm Hg in cold nebulized and 91 mm Hg leads to 61 mm Hg in warm nebulized) and mean pHa (7.43 leads to 7.23 in cold nebulized and 7.42 leads to 7.31 in warm nebulized). All rabbits in the control and warm humidified groups survived the study whereas 9 of 22 in the nebulized groups died before completion of study (P < 0.005). Morphometric analysis revealed a significant increase in the mean vascular wall thickness in both nebulized groups of rabbits when compared to that in the control and warm humidified groups (P < 0.05). The cold nebulized group also had significantly less air space and correspondingly more interstitial thickness and intraalveolar edema (P < 0.05) compared to control and warm humidified groups. These findings of pulmonary parenchymal damage in rabbits ventilated with air containing particulate water and the greater degree of both physiologic and anatomic change evident in the cold nebulized animals suggest that particulate water and low inspired air temperature may contribute to the genesis of pulmonary damage during intermittent positive pressure ventilation.
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