Persistence of coronary vasodilator reserve despite functionally significant flow reduction

This study was done to determine whether coronary vasodilator reserve is exhausted when coronary flow falls and regional function becomes abnormal during low-pressure perfusion. In 10 open-chest, anesthetized dogs the left circumflex coronary artery (LC) was cannulated and perfused via a blood-filled reservoir. At LC pressures of 35 and 50 mmHg, regional segment lengths were measured with sonomicrometer crystals and regional flow with radiolabeled microspheres before and after adenosine vasodilation. Control measurements were made at 80 mmHg perfusion pressure. Prior to adenosine, flow fell transmurally when LC pressure was reduced to 50 and 35 mmHg and rose significantly following adenosine. No change in function occurred at an LC pressure of 50 mmHg, but at 35 mmHg LC segmental shortening fell to 30 ± 14% of control, and LC flow fell to 42 ± 5% of control, with endocardial and epicardial flows of 0.40 ± 0.04 and 0.70 ± 0.09 ml·min^-1·g^-1, respectively. After adenosine, endocardial and epicardial LC flow rose to 0.69 ± 0.08 and 1.81 ± 0.47 ml·min^-1·g^-1, respectively (P < 0.05). LC segment shortening improved modestly to 50 ± 15% of control (P < 0.02). We conclude that transmural vasodilator reserve is maintained in the face of functionally significant reductions of coronary flow at low perfusion pressure. Adenosine-induced flow increases are associated with a modest improvement in segmental function.