Wall tension and myocardial dysfunction after ischemia and reperfusion

Systolic stresses on non-contracting myocardial segments were induced in isolated rabbit hear preparations to investigate the observed difference in the restoration of cardiac functions after ischemic stress on hearts in vivo or in vitro. Results indicate that ischemia lasting for 30 minutes or less causes extensive damage to dyskinetic hearts. Adenosine triphosphate store and oxygen consumption is reduced even after reperfusion. Cardiac wall stiffness was also elevated to three times the normal. This indicate that the mechanical stress resulting from dyskinesia add significantlyto the damage caused by ischemia.