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-supported 45Ca2+ transport compared with sarcoplasmic reticulum from normal myocardium (0.93 vs. 1.12 μmol 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 μmol P(i)/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 inabillity of the stunned heart to maintain normal mechanical function.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine