Mechanisms of airway hyper-responsiveness after coronary ischemia

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. Zrs was determined under baseline conditions, and following iv boluses of 20 and 30 mu g/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 Raw but led to bronchial hyper-reactivity (BHR) with 2.7 +/- 0.5-times (p < 0.05) greater responses in Raw to 30 mu g/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. (c) 2008 Elsevier B.V. All rights reserved.