Key result
Propranolol significantly limited myocardial infarct size in dogs with reperfusion (4.6% vs 22.6% with saline), but was ineffective in the absence of reperfusion.
Why the study?
Does propranolol reduce myocardial infarct size in a canine model of coronary occlusion with and without reperfusion?
Does propranolol reduce myocardial infarct size in a canine model of coronary occlusion with and without reperfusion?
Absolute Event Rate: 4.6% vs 22.6%
Propranolol limits myocardial infarct size in a canine model only when administered in the setting of coronary reperfusion, either before occlusion or after reperfusion initiation.
Propranolol may limit infarct size with reperfusion in canine models; leaves open translation to human reperfusion therapy.
The ability of propranolol to limit myocardial infarct size (IS) following coronary artery occlusion with and without reperfusion into a critical stenosis was assessed in the dog. IS was determined by the nitrobluetetrazolium staining method and expressed as percent of the left ventricle (free wall plus septum). In Series 1 dogs the left circumflex coronary artery (LCX) was ligated at its origin. IS at 6 h was similar in groups pretreated with saline (36.0 +/- 1.3%) or propranolol (0.2 mg . kg-1, 34.7 +/- 1.7%; 1.0 mg . kg-1, 36.7 +/- 1.5%; 4.4 mg . kg-1, 34.8 +/- 0.3%). In Series 2 dogs a relatively small infarction was produced by ligating the largest branch of the LCX between the left anterior descending and posterior descending arteries. IS at 6 h was not significantly different in dogs pretreated with saline (8.1 +/- 1.7%) or propranolol (0.2 mg . kg-1, 7.1 +/- 2.5%; 1.0 mg . kg-1, 4.6 +/- 1.2%). In Series 3 dogs the LCX was ligated approximately 10 mm from its origin for 60 min followed by reperfusion into a critical stenosis. IS determined at 24 h was significantly less in dogs treated with propranolol (1.0 mg . kg-1) before LCX occlusion (4.6 +/- 0.6%) or 5 min after LCX reperfusion (9.5 +/- 1.8%) than in dogs treated with saline (22.6 +/- 2.8%). In Series 4 dogs treatment was exactly as in Series 3 except that reperfusion was not instituted. IS was similar in dogs pretreated with saline (29.0 +/- 1.5%) or propranolol (31.1 +/- 3.0%). Thus, in the present study, propranolol limited IS in the presence but not in the absence of reperfusion. In the reperfusion model propranolol was effective when administered before coronary occlusion or after initiation of reperfusion.
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Reynolds et al. (1981) studied Myocardial infarction. Propranolol vs. Saline was evaluated on Myocardial infarct size (percent of left ventricle). Propranolol significantly limited myocardial infarct size in dogs with reperfusion (4.6% vs 22.6% with saline), but was ineffective in the absence of reperfusion.
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