Reversal of the no reflow phenomenon in globally ischemic rat hearts by ventricular dilation.

Changes in the contracture and stiffness of ventricular walls during ischemia and their effect on vascular reperfusion were studied in isolated rat hearts. Global ischemia was induced by stopping the flow of oxygenated perfusate for 60 min. Contracture pressures generated against water-filled left ventricular balloons maintained at diastolic volume increased between 8 and 25 min of ischemia and declined thereafter. On the other hand, left ventricular wall stiffness, estimated from the pressure required to periodically inflate otherwise uninflated balloons to diastolic volume, increased rapidly between 20 and 30 min of ischemia, and more slowly thereafter. Inflation of balloons following 30 or more min of ischemia caused significant reductions in left ventricular wall stiffness. Similar brief inflation after 60 min of ischemia allowed aqueous sodium fluorescein to perfuse the subendocardial half of the left ventricular wall which was otherwise not accessible to reperfusion. This reversal of the no reflow phenomenon was accompanied by a reduction in myocardial wall stiffness, stretching of myocytes and increased patency of myocardial capillaries.