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.