We investigated the development of pulmonary inflammation and pulmonary vascular hypertrophy induced by continuous catecholamine (CA) infusion in rats. We studied the role of proinflammatory cytokines in this pathogenetic process and their relationship to pulmonary injury and to cardiac hypertrophy. Female Sprague-Dawley rats (n=251) received a continuous intravenous infusion of norepinephrine (NE), phenylephrine (PE), isoproterenol (ISO) or NaCl 0.9% (as control) over time intervals between 20 min and 72 h. We analysed cardiac function and hypertrophy as well as activation of proinflammatory cytokines in lung, serum, pleural fluid and bronchoalveolar lavage (BAL) fluid. Additionally, BAL cytology and histologic changes in the lung were investigated. Lung histology showed pulmonary oedema, inflammation and vascular hypertrophy after stimulation with all types of CA. In the lung, mRNA of IL-1α, IL-1β and IL-6, but not of TNFα, increased transiently after 45 min of PE and, to a lower degree, ISO infusion. Only PE infusion induced accumulation of neutrophils and macrophages in BAL. The degrees of pulmonary inflammation and vascular hypertrophy were similar with different stimulation types, and there was a significant positive correlation between these two processes. Right ventricular (RV) hypertrophy was induced by ISO but not by PE. These results demonstrate that CA elicit pulmonary inflammation and thereby, pulmonary vascular hypertrophy. Both α- and β-adrenergic mechanisms have been shown to contribute to this pathogenesis. However, it is likely that RV hypertrophy developed as a consequence of direct CA effects rather than of pulmonary vascular hypertrophy.