Isoproterenol or aminophylline attenuate pulmonary edema after acid lung injury.

We tested the hypothesis that isoproterenol and aminophylline would reduce both the pulmonary hypertension and increased pulmonary vascular permeability caused by the intratracheal instillation of hydrochloric acid. The lungs of New Zealand white rabbits were studied using a blood-perfused isolated lung preparation. Changes in pulmonary artery pressure and lung weight were measured for 30 min after acid injury (2 ml/kg 0.1 N HCl). In a control group without acid injury, pulmonary artery pressure and lung weight did not change throughout 1 h of perfusion. In an acid control group, pulmonary artery pressure increased 11 +/- 3 mmHg (p less than 0.01), and lung weight increased 19.2 +/- 5.1 g during the 30 min after acid injury (p less than 0.001). Pretreatment with aminophylline (p less than 0.01) or isoproterenol (p less than 0.001) completely prevented the increase in pulmonary artery pressure after acid instillation. Pretreatment with aminophylline strikingly reduced the increase in lung weight caused by acid injury to 3.6 +/- 1.0 g over 30 min (p less than 0.01). Pretreatment with isoproterenol prevented any increase in lung weight (0.5 +/- 0.5 g over 30 min, p less than 0.01). Post-treatment with isoproterenol beginning 3 min after acid instillation also prevented the increase in pulmonary artery pressure (p less than 0.01) and markedly reduced the increase in lung weight to 5.8 +/- 2.4 g over 30 min (p less than 0.01). The beneficial effect of isoproterenol is mediated through activation of beta-adrenergic receptors because propranolol reverses its effect.(ABSTRACT TRUNCATED AT 250 WORDS)