We explored the consequences of myocardial ischemia (MI) on the lung responsiveness and identified the pathophysiological mechanisms involved. Airway resistance (R(aw)) was identified from the respiratory system input impedance (Z(rs)) in rats. Z(rs) was determined under baseline conditions, and following iv boluses of 20 and 30 microg/kg serotonin. MI was then induced in the animals in Group I by ligating the left-interventricular coronary artery, while rats in Group C underwent sham surgery. Four weeks later, baseline Z(rs) and its changes following serotonin administration were reassessed. Lung morphological changes were assessed by histology, and alpha smooth muscle actin cells (alpha-SMA) were identified. MI induced no changes in baseline R(aw) but led to bronchial hyper-reactivity (BHR) with 2.7+/-0.5-times (p<0.05) greater responses in R(aw) to 30 microg/kg serotonin. Perivascular edema and alpha-SMA cell proliferation were observed after MI. The development of BHR following MI is a consequence of the expression of alpha-SMA, while the geometrical alterations caused by the pulmonary vascular engorgement have smaller impact.