&NA;This study examined the possibility that the postischemic mechanical depression observed in the “stunned” myocardium is a result of an alteration in the control of intracellular calcium. Regional myocardial stunning was produced in five open‐chest dogs by eight to twelve 5‐minute occlusions of the left anterior descending coronary artery, alternated with 10‐minute reflow periods and followed by a final 60‐minute period of reperfusion. Systolic segment shortening in the postischemic zone, measured by sonomicrometry, fell from 14.9% at baseline to −1.1% at the end of reperfusion. Sarcoplasmic reticulum isolated from stunned myocardium demonstrated a 17% reduction in oxalate‐supported45Ca2+transport compared with sarcoplasmic reticulum from normal myocardium (0.93 vs. 1.12 &mgr;mol Ca2+/mg protein/min,p<0.005). There was also a 20% decrease in the maximal activation by Ca2+of the sarcoplasmic reticulum Ca2+,Mg2+‐ATPase (2.46 vs. 1.96 &mgr;mol Pi/mg protein/min,p<0.005), and a downward shift in the Ca2+‐activation curve of the Ca2+,Mg2+‐ATPase. These results indicate that myocardial stunning is associated with damage to the calcium‐transport system of the sarcoplasmic reticulum. Altered intracellular control may contribute to the inability of the stunned heart to maintain normal mechanical function. (Circulation Research1989;65:526‐530)