Key result
In a canine model of myocardial ischemia, the alpha1-blocker bunazosin prolonged the shortened epicardial refractory period and reduced transmural dispersion, whereas the beta-blocker propranolol increased transmural dispersion in the ischemic area.
Why the study?
Does alpha-1 or beta-adrenoceptor blockade alter the refractory period and myocardial blood flow in ischemic myocardium in a canine model?
Does alpha-1 or beta-adrenoceptor blockade alter the refractory period and myocardial blood flow in ischemic myocardium in a canine model?
In a canine model of acute myocardial ischemia, alpha-1 blockade with bunazosin reduced the dispersion of refractoriness between endocardial and epicardial layers, whereas beta-blockade with propranolol increased it, suggesting different electrophysiological mechanisms.
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Usui et al. (1998) studied Myocardial ischemia (n=32). Bunazosin and Propranolol vs. Control (saline) was evaluated on Refractory period and myocardial blood flow in ischemic and normal myocardium. In a canine model of myocardial ischemia, the alpha1-blocker bunazosin prolonged the shortened epicardial refractory period and reduced transmural dispersion, whereas the beta-blocker propranolol increased transmural dispersion in the ischemic area.
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