Although ischemia induces strong coronary vasodilation, some vasoconstrictive tone persists in the ischemic myocardium. To assess whether this tone is mediated through alpha adrenergic receptors, coronary blood flow was measured with radioactive microspheres in the normal and in the ischemic left ventricular wall of the dog before and during alpha blockade with Trimazosin. Ischemia was accomplished by decreasing the coronary perfusion pressure to 22 +/- 1.4 mmHg. Heart rate and aortic pressure were kept constant in each experiment. Trimazosin significantly increased flow in the normal left ventricular wall, but to a greater extent in the subepicardium than in the subendocardium with a decrease of the inner/outer flow ratio from 1.38 +/- 0.12 to 1.20 +/- 0.11 (p less than 0.05). In the ischemic region, Trimazosin did not change total transmural flow, but flow decreased in the subendocardium and increased in the subepicardium with a decrease in the inner/outer flow ratio from 0.63 +/- 0.09 to 0.38 +/- 0.06 (p less than 0.01). These results show that a vasoconstrictive tone mediated through alpha-1 adrenergic receptors persists in the ischemic myocardium, the blockade of which is detrimental for the subendocardium.