ASPIRATION PNEUMONIA - TREATMENT WITH PULMONARY VASODILATORS
- 1 January 1983
- journal article
- research article
- Vol. 94 (1) , 95-99
Abstract
Experimental aspiration pneumonia induced in the isolated perfused ventilated canine pulmonary lobe by the intrabronchial instillation of HCl is characterized by pulmonary edema, intrapulmonary shunting and loss of lung compliance. Pulmonary artery pressure also increases. In an attempt to modify the injury response, the increase in pulmonary artery pressure in the isolated lobe model was restricted by administering vasodilator drugs. In control lobes perfused for 4 h there was minimal weight gain (14 g), pulmonary artery pressure remained stable (13 mm Hg) and intrapulmonary shunting did not occur. Following intrabronchial instillation of 0.2 ml of 0.1 N HCl/g of lobe wt, lobe wt tripled (183 g), pulmonary artery pressure (20 mm Hg) was significantly increased and significant intrapulmonary shunting (32%) developed. When sodium nitroprusside (2 .mu.g/min per kg of dog body wt) was infused into the pulmomary artery 3 min 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 g) and intrapulmonary shunting (15%) compared to untreated acid lobes. When isoproterenol (0.04 .mu.g/min per kg dog body wt) 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 accompanied by a significant reduction in weight gain (60 g) and intrapulmonary shunting (6%) compared to untreated acid lobes. The increase in the pulmonary artery pressure following acid injury can evidently be lowered pharmacologically and a significant decrease in injury response follows. The magnitude of the injury response is apparently in part a function of pulmonary artery pressure.This publication has 0 references indexed in Scilit: