Left ventricular performance at high end-diastolic pressures in isolated, perfused dog hearts.

Abstract

In the isolated, blood-perfused heart of the dog, left ventricular developed pressure and developed mean wall stress were observed while the ventricle contracted at a constant, nearly isovolumic afterload and while end-diastolic pressure was raised to levels exceeding 100 mm Hg. Coronary perfusion pressure was maintained at the level of the peak systolic pressure. Dilatation of the mitral ring and consequent mitral regurgitation were avoided by left atrial plication. Normalized graphs of percent of peak developed pressure against end-diastolic pressure showed that developed pressure rose abruptly with diastolic pressure, peaked at a diastolic pressure of approximately 30 mm Hg, and declined 14.7% (±0.9 SE) at an end-diastolic pressure of 100 mm Hg. Likewise, developed mean wall stress rose abruptly with diastolic pressure, peaked at a higher diastolic pressure of approximately 50 mm Hg, and declined only 7.5% (±0.8 SE) from this peak at an end-diastolic pressure of 100 mm Hg. Similar findings were observed in hearts acutely depressed with propranolol. Electron micrographs showed sarcomere length to average 2.275µ and 2.300µ in ventricles fixed in diastole while subjected to pressures of 61 and 100 mm Hg, respectively, after potassium arrest, confirming the findings illustrated by the normalized graphs. These observations imply that in the isolated heart of the dog there is no loss of ventricular performance attributable to a descending limb of the Frank-Starling mechanism until the end-diastolic pressure exceeds 60 mm Hg and that this loss is minimal at diastolic pressures as high as 100 mm Hg.