In an isolated rat heart perfused with an oxygenated solution, reducing atrial inflow would cause what change in force of contraction and cardiac output?

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In an isolated heart that’s perfused retrogradely through the aorta, atrial venous return doesn’t set the ventricular preload. The ventricle’s filling is driven by the externally supplied perfusate and the pressure in the perfusion circuit, not by the amount of atrial inflow. Therefore, reducing atrial inflow doesn’t change the end-diastolic volume of the ventricle, so the stretch of the cardiac muscle—and thus the force of contraction via preload—remains essentially the same. With the contraction strength unchanged and the perfusion maintaining output, the overall cardiac output doesn’t change either. In contrast, in a whole animal, reduced venous return would lower preload and CO, but in this isolated perfused heart setup, atrial inflow isn’t the limiting factor, so no change occurs.