Pulmonary morphofunctional effects of acute myocardial infarction

Acute myocardial infarction (AMI) may yield several respiratory changes. Ne vertheless, no comprehensive pulmonary morphological/physiological correlat ion has been performed under this condition. The aims of the present invest igation were: 1) to determine the respiratory parameters in an experimental model of coronary artery occlusion, 2) to relate these results to findings from lung histopathology, and 3) to evaluate the effects of propranolol us ed prior to AMI. Twenty-eight rats were anaesthetized and mechanically ventilated. In the co ntrol group (C), a suture line was passed around the left anterior descendi ng coronary artery (LADCA). The infarct group (I) was similarly prepared bu t the LADCA was Ligated and infarct resulted. In the control/propranolol (C P) and infarct/propranolol (IP) groups, propranolol was intravenously injec ted 5 min before surgery as performed in groups C and I, respectively. Lung static (EL,st) and dynamic (EL,dyn) elastances, airway resistance (RL,int) , and viscoelastic/inhomogeneous pressure (Delta P2L) were determined befor e and 30, 60 and 120 min after surgery. In group I, EL,st, EL,dyn, RL,int and Delta P2L increased progressively thr oughout the experiment, and were higher than those found in groups C, CP an d IP. All respiratory parameters but EL,st remained unaltered in group IF. Lung histopathological examination demonstrated alveolar, interstitial and intrabronchial oedema in group I. Group IP showed only interstitial oedema. Acute myocardial infarction yields lung resistive, elastic and viscoelastic changes. The last two results from alveolar and interstitial oedema, respe ctively. The previous use of propranolol diminishes respiratory changes.