Aspiration pneumonia: treatment with pulmonary vasodilators.

Experimental aspiration pneumonia induced in the isolated perfused ventilated canine pulmonary lobe by the intrabronchial instillation of hydrochloric acid is characterized by pulmonary edema, intrapulmonary shunting, and loss of lung compliance. In addition, pulmonary artery pressure increases. In an attempt to modify the injury response, we restricted the increase in pulmonary artery pressure in the isolated lobe model by administering vasodilator drugs. In control lobes perfused for 4 hours there was minimal weight gain (14 gm), pulmonary artery pressure remained stable (13 mm Hg), and intrapulmonary shunting did not occur. Following intrabronchial instillation of 0.2 ml of 0.1N HCl/gm of lobe weight, lobe weight tripled (183 gm), pulmonary artery pressure (20 mm Hg) was significantly increased, and significant intrapulmonary shunting (32%) developed. When sodium nitroprusside (2 micrograms/min/kg of dog body weight) was infused into the pulmonary artery 3 minutes after HCl instillation, the pulmonary artery pressure was significantly reduced (13 mm Hg) compared to that in untreated acid lobes. This was accompanied by a significant reduction in mean weight gain (100 gm) and intrapulmonary shunting (15%) compared to untreated acid lobes. Similarly, when isoproterenol (0.04 micrograms/min/kg dog body weight) was infused into the pulmonary artery following acid instillation, the pulmonary artery pressure (12.5 mm Hg) was significantly reduced compared to that in untreated acid lobes. This was also accompanied by a significant reduction in weight gain (60 gm) and intrapulmonary shunting (6%) compared to untreated acid lobes. These data demonstrate that the increase in pulmonary artery pressure following acid injury can be lowered pharmacologically and that a significant decrease in injury response follows. This suggests that the magnitude of the injury response is in part a function of pulmonary artery pressure.