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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 less than 0.05). LC segment shortening improved modestly to 50 +/- 15% of control (P less than 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.

The influence of afterload resistance on the end-systolic pressure-thickness relationship (ESPTR) was assessed in six isolated canine left ventricles made to eject into a simulated arterial system. An increase of simulated peripheral resistance from 1.5 to 6.0 mmHg.s.ml-1 resulted in a modest but significant shift of the ESPTR upward and to the right, indicating augmented contractile performance. A relationship between the extent of systolic wall thickening and end-systolic performance was also observed: increased wall thickening impairing and decreased wall thickening enhancing end-systolic performance. The dependence of end-systolic performance on wall thickening history in this setting is consistent with shortening deactivation. This phenomenon appears to account at least in part for the observed shift in the ESPTR with altered afterload resistance.