Influence of terbutaline on endotoxin-induced lung injury

The effects of the beta-2-receptor agonist terbutaline on central hemodynamics, gas exchange, and platelet and leukocyte counts during 3 hr of endotoxin shock were studied. Ten sheep were anesthetized and ventilated without positive end-expiratory pressure (PEEP). After 1 hr of stabilization (t = -30), five animals (Group T) received intravenous (i.v.) infusion of terbutaline, 20 micrograms/kg/hr for 3.5 hr, whereas the other five received no drug treatment and served as controls (Group C). Thirty min later (t = 0) all animals received Escherichia coli endotoxin 10 micrograms/kg by i.v. infusion over 15 min. The terbutaline infusion increased the heart rate (HR) initially by 30% and the cardiac index (CI) by 50%, whereas mean arterial pressure (MAP), pulmonary artery pressure (PAP), and gas exchange remained unchanged. Terbutaline pretreatment did not prevent the pulmonary hypertension that characteristically occurs after endotoxin injection, nor did it decrease the initial fall in platelet count, leukocyte count, arterial oxygen tension (PaO2), or respiratory compliance (t = 30). However, during the permeability phase (after 120-180 min), there was a significant improvement in MAP, PAP, respiratory compliance, PaO2, and arterial pH in the animals treated with terbutaline as compared with the control animals. Also, the wet weight to dry weight ratio of the lungs from animals receiving terbutaline was significantly lower than in controls. It was concluded that terbutaline does not influence the hypertension phase during endotoxin shock, but it may decrease pulmonary microvascular leakage during the permeability phase.